Grypa świńska (h1n1)
Patofizjologia i mechanizm

Wirus grypy świńskiej H1N1, będący podtypem wirusa grypy A z rodziny Orthomyxoviridae, charakteryzuje się jednoniciowym, segmentowanym genomem RNA o ujemnej polarności. Pandemia z 2009 roku była wynikiem tzw. „poczwórnej reasortacji” genetycznej, łączącej segmenty wirusów ptasich, ludzkich oraz dwóch linii świńskich, co umożliwiło efektywną transmisję między ludźmi. Tropizm wirusa pandemicznego H1N1 obejmuje zarówno górne, jak i dolne drogi oddechowe, w tym tchawicę, oskrzela i oskrzeliki, co różni go od sezonowych szczepów replikujących się głównie w jamie nosowej. Okres inkubacji wynosi średnio 2 dni (zakres 1-7 dni). Patogeneza obejmuje uszkodzenie nabłonka dróg oddechowych, martwicę, złuszczanie komórek oraz rozlane uszkodzenie pęcherzyków płucnych, co prowadzi do klinicznych objawów grypy i powikłań, takich jak pierwotne wirusowe lub wtórne bakteryjne zapalenie płuc. W ciężkich przypadkach obserwuje się także zatorowość płucną i inne powikłania zakrzepowo-zatorowe.

Patogeneza wirusa grypy świńskiej (H1N1)

Grypa świńska (H1N1) to choroba zakaźna układu oddechowego wywołana przez podtyp wirusa grypy A. Wirus ten początkowo zakaził trzodę chlewną, ale w wyniku procesów rekombinacji genetycznej nabrał zdolności do zakażania ludzi i efektywnej transmisji między nimi, co doprowadziło do globalnej pandemii w latach 2009-2010.12

Charakterystyka wirusa H1N1

Wirus grypy H1N1 należy do rodziny Orthomyxoviridae i posiada jednoniciowy, segmentowany genom RNA o ujemnej polarności.1 Nazwa H1N1 pochodzi od dwóch głównych glikoprotein powierzchniowych wirusa: hemaglutyniny (H) i neuraminidazy (N), które odgrywają kluczową rolę w patogenezie zakażenia.12

Pandemia H1N1 z 2009 roku była spowodowana przez nowy szczep wirusa, który powstał w wyniku tzw. „poczwórnej reasortacji” genetycznej, łączącej materiał genetyczny wirusów grypy pochodzenia ptasiego, ludzkiego oraz dwóch różnych linii świńskich (północnoamerykańskiej i eurazjatyckiej).12 Świnie są uważane za „naczynie mieszające” dla wirusów grypy, ponieważ ich komórki posiadają receptory zarówno dla wirusów ptasich, jak i ssaków, co zwiększa możliwość wymiany segmentów genetycznych między różnymi szczepami.12

Mechanizm zakażenia komórek gospodarza

Proces zakażenia wirusem H1N1 rozpoczyna się w górnych drogach oddechowych i przebiega w kilku etapach:12

  1. Przyłączenie wirusa do komórki gospodarza – hemaglutynina (H) wirusa wiąże się z receptorami zawierającymi kwas sialowy na powierzchni komórek nabłonkowych dróg oddechowych
  2. Endocytoza – wirus wnika do komórki poprzez receptor-mediowaną endocytozę, tworząc endosom zawierający wirion
  3. Fuzja błon – hemaglutynina pośredniczy w fuzji błony endosomu z otoczką wirusa, co prowadzi do uwolnienia nukleokapsydu wirusa do cytoplazmy
  4. Replikacja – wirus wykorzystuje maszynerię komórkową do powielania swojego materiału genetycznego i produkcji białek wirusowych
  5. Składanie i uwalnianie – nowo powstałe cząstki wirusowe są składane i uwalniane z komórki poprzez pączkowanie, przy czym neuraminidaza (N) odgrywa kluczową rolę w uwalnianiu wirionów poprzez rozcinanie receptorów kwasu sialowego

Neuraminidaza jest szczególnie istotna w fazie uwalniania wirusa, gdyż rozszczepia receptory kwasu sialowego, co zapobiega agregacji cząstek wirusowych i umożliwia ich rozprzestrzenianie się do sąsiednich komórek.12

Replikacja i rozprzestrzenianie się w organizmie

Replikacja wirusa H1N1 zachodzi głównie w komórkach nabłonkowych górnych i dolnych dróg oddechowych. Okres inkubacji dla wirusa grypy H1N1 z 2009 roku wynosi średnio 2 dni (zakres 1-7 dni).1

Wirus grypy H1N1 wykazuje tropizm do komórek nabłonka dróg oddechowych i już w ciągu 16 godzin od zakażenia rozpoczyna namnażanie w nabłonku oskrzelowym.1 W przeciwieństwie do sezonowej grypy H1N1, która zazwyczaj replikuje się głównie w jamie nosowej, wirus pandemiczny H1N1 z 2009 roku wykazuje zdolność do replikacji również w tchawicy, oskrzelach i oskrzelikach, co może tłumaczyć jego zwiększoną zjadliwość.1

Badania na modelach zwierzęcych wykazały, że wirus H1N1 z 2009 roku replikował się do wyższych mian w tkance płucnej i był izolowany z przewodu pokarmowego zwierząt zakażonych donosowo, czego nie obserwowano w przypadku sezonowego wirusa H1N1.1 Sugeruje to, że wirus pandemiczny H1N1 może powodować bardziej rozległe zakażenie organizmu niż sezonowe szczepy grypy.

Zmiany patologiczne w tkankach

Zakażenie wirusem H1N1 prowadzi do charakterystycznych zmian patologicznych w układzie oddechowym, które wyjaśniają objawy kliniczne grypy świńskiej.1

Zmiany w nabłonku oddechowym

Wirus H1N1 infekuje i niszczy komórki nabłonka dróg oddechowych, powodując:12

  • Ogniskową martwicę nabłonka oskrzelowego
  • Złuszczanie się martwych komórek nabłonka do światła dróg oddechowych
  • Zastąpienie nabłonka walcowatego komórkami spłaszczonymi i metaplastycznymi
  • Obrzęk i przekrwienie błony podśluzowej

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W ciągu 24-48 godzin od zakażenia można zaobserwować charakterystyczne mikroskopowe zmiany w postaci martwiczego zapalenia oskrzelików. W kolejnych 2-3 dniach pozostałe komórki nabłonkowe spłaszczają się pokrywając błonę podstawną (atenuacja), a następnie zaczynają się namnażać, tworząc warstwy (hiperplazja).1

Zmiany w płucach

W płucach zakażenie H1N1 może prowadzić do poważniejszych zmian patologicznych, szczególnie w przypadku ciężkiego przebiegu choroby:12

  • Obrzęk śródmiąższowy z naciekami zapalnymi
  • Wysięk białkowy w pęcherzykach płucnych z tworzeniem błon szklistych
  • Zakrzepica naczyń włosowatych
  • Martwica przegród pęcherzykowych
  • Krwotoki śródpęcherzykowe
  • Rozlane uszkodzenie pęcherzyków płucnych z naciekiem limfocytów i histiocytów w śródmiąższu

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W badaniach na modelu mysim wykazano, że wirus H1N1 z 2009 roku powodował łagodne do umiarkowanego zapalenie oskrzelików z okazjonalną martwicą nabłonka oskrzelików i łagodnym do umiarkowanego zapaleniem pęcherzyków płucnych wokół oskrzelików.1 Jednak te zmiany były mniej nasilone w porównaniu z wysoce patogennymi wirusami, takimi jak zrekonstruowany wirus grypy z 1918 roku czy wysoce patogenne wirusy grypy ptaków H5N1.2

Odpowiedź immunologiczna i burza cytokinowa

Interakcja między wirusem H1N1 a układem odpornościowym gospodarza jest kluczowym elementem patogenezy grypy świńskiej.1

Wrodzona odpowiedź immunologiczna

Po zakażeniu wirusem H1N1 aktywowana jest wrodzona odpowiedź immunologiczna, obejmująca:12

  • Aktywację szlaków wykrywających wirusy, w tym receptorów toll-podobnych (TLR), receptorów RIG-I-podobnych (RLR) i receptorów NOD-podobnych (NLR)
  • Uruchomienie szlaków sygnałowych NF-κB i JAK-STAT
  • Produkcję interferonów typu I, które indukują stan przeciwwirusowy w komórkach sąsiadujących
  • Wydzielanie cytokin prozapalnych, takich jak IL-1β, IL-6 i TNF-α

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Badania wykazały, że w porównaniu z sezonowymi szczepami, wirus pandemiczny H1N1 może wywoływać silniejszą odpowiedź immunologiczną, co może przyczyniać się do jego zwiększonej patogenności.1

Burza cytokinowa

Burza cytokinowa to nadmierna odpowiedź układu immunologicznego, która może wystąpić w ciężkich przypadkach zakażenia H1N1. Jest to ogólnoustrojowa ekspresja zdrowego i silnego układu odpornościowego, prowadząca do uwolnienia ponad 150 mediatorów zapalnych (cytokin, wolnych rodników tlenowych i czynników krzepnięcia).1

Zarówno cytokiny prozapalne (takie jak TNF-α, IL-1 i IL-6), jak i przeciwzapalne (takie jak IL-10 i antagonista receptora IL-1) są podwyższone w surowicy, a ich gwałtowna i często śmiertelna interakcja określana jest jako „burza cytokinowa”. Główny udział w jej rozwoju mają TNF-α i IL-6.1

Burza cytokinowa to nieprawidłowa (przesadna) odpowiedź immunologiczna, spowodowana przez szybko namnażające się i wysoce aktywowane limfocyty T lub komórki NK (Natural Killer). W przypadku pandemii grypy z 1918 roku, niezwykle wysoka śmiertelność mogła być częściowo spowodowana właśnie burzą cytokinową, która prowadziła do nadmiernej stymulacji układu odpornościowego.1

Odpowiedź adaptacyjna

Odpowiedź adaptacyjna na zakażenie wirusem H1N1 obejmuje:1

  • Aktywację limfocytów T CD4+ – następująca bezpośrednio po zakażeniu
  • Ekspansję populacji limfocytów T CD4+ i CD8+ – nasilającą się w okresie 3-7 dni po zakażeniu, co zbiega się z pojawieniem objawów klinicznych
  • Produkcję przeciwciał swoistych dla nukleoprotein i hemaglutyniny H1 – wykrywalnych już 7 dni po zakażeniu

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Zrozumienie odpowiedzi immunologicznej na zakażenie H1N1 jest kluczowe dla opracowania skutecznych metod leczenia i zapobiegania ciężkim powikłaniom grypy świńskiej.

Czynniki wpływające na wirulencję i transmisję

Różne szczepy wirusa H1N1 wykazują zróżnicowaną wirulencję i zdolność do transmisji, co jest uwarunkowane wieloma czynnikami molekularnymi.12

Adaptacja genetyczna wirusa

Kluczowe dla wirulencji i transmisji wirusa H1N1 są następujące cechy:12

  • Mutacje w polimeraze wirusa – odkryto mutację określaną jako polimorfizm SR, która zwiększa zdolność replikacji wirusa w komórkach ludzkich
  • Zdolność wiązania receptorów – hemaglutynina wirusa H1N1 z 2009 roku wykazuje powinowactwo do receptorów zawierających kwas sialowy człowieka
  • Białka niestrukturalne – białka NS1 i PB1-F2 przyczyniają się do wirulencji poprzez wpływ na apoptozę, tłumienie odpowiedzi interferonowej, zwiększenie szybkości replikacji wirusa i opóźnienie usuwania wirusa oraz nasilenie stanu zapalnego

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Badania wykazały, że wirus H1N1 z 2009 roku zawierał konfiguracje receptorów wiążących (pozycja Q223 i G225 w HA1), które wskazują na powinowactwo do receptorów ssaków, co mogło przyczynić się do jego efektywnej transmisji między ludźmi.1

Zmienność genetyczna wirusa

Wirusy grypy, w tym H1N1, podlegają dwóm głównym mechanizmom zmienności genetycznej:1

  • Przesunięcie antygenowe (antigenic shift) – mechanizm, w którym dwa lub więcej szczepów wirusa tworzą zupełnie nowy szczep poprzez współzakażenie komórki i wymianę całych segmentów materiału genetycznego (H i/lub N w przypadku grypy). Powstały nowy szczep posiada zupełnie nowe antygeny, co sprawia, że populacja jest na niego wrażliwa.
  • Dryf antygenowy (antigenic drift) – mechanizm zmienności wirusów, który polega na akumulacji mutacji w genach kodujących miejsca wiązania przeciwciał. W efekcie powstaje nowy szczep cząstek wirusa, który nie może być skutecznie hamowany przez przeciwciała skierowane przeciwko wcześniejszym szczepom, co ułatwia rozprzestrzenianie się wirusa w częściowo odpornej populacji.

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Pandemia H1N1 z 2009 roku była wynikiem przesunięcia antygenowego, w którym nowy wirus powstał z połączenia materiału genetycznego wirusów grypy świńskiej, ptasiej i ludzkiej.1

Czynniki wpływające na transmisję

Transmisja wirusa H1N1 między ludźmi zachodzi głównie poprzez:12

  • Kropelki wydzieliny dróg oddechowych – uwalniane podczas kaszlu, kichania, mówienia czy oddychania
  • Kontakt bezpośredni – z osobą zakażoną
  • Kontakt pośredni – z zanieczyszczonymi powierzchniami, a następnie dotykanie ust, nosa lub oczu

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Osoby zakażone mogą rozprzestrzeniać wirusa od około jednego dnia przed wystąpieniem objawów do około 4-7 dni po ich pojawieniu się, co znacznie utrudnia kontrolę zakażeń.12

Badania na modelach zwierzęcych wykazały, że wirus H1N1 z 2009 roku wykazywał mniej efektywną transmisję drogą kropelkową w porównaniu z wysoce zakaźnym fenotypem sezonowego wirusa H1N1, pomimo jego zwiększonej replikacji w układzie oddechowym.1

Powikłania i mechanizmy rozwoju choroby ciężkiej

Zakażenie wirusem H1N1 może prowadzić do różnych powikłań, szczególnie u osób z grup ryzyka.1

Powikłania płucne

Najpoważniejszym powikłaniem grypy świńskiej jest zapalenie płuc, które może rozwinąć się na dwa sposoby:1

  • Pierwotne wirusowe zapalenie płuc – spowodowane bezpośrednio przez wirusa H1N1, charakteryzujące się szybkim postępem i ciężkim przebiegiem
  • Wtórne bakteryjne zapalenie płuc – infekcja bakteryjna nakładająca się na uszkodzenie tkanek spowodowane przez wirusa

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Badania wykazały, że zakażenie H1N1 może wywoływać zator płucny, co sugeruje się jako główną przyczynę zgonów w pandemii z 2009 roku. Lekarze powinni rozważyć wykonanie tomografii komputerowej ze wzmocnieniem kontrastowym w celu oceny obecności zatorów płucnych u pacjentów z powikłaniami oddechowymi w „ciężkich” przypadkach grypy H1N1.1

Powikłania pozapłucne

H1N1 może wywoływać również inne powikłania zakrzepowo-zatorowe, takie jak:1

  • Zawał mięśnia sercowego
  • Obustronna masywna zakrzepica żył głębokich
  • Zakrzep tętnicy aorty podnerkowej
  • Zakrzepica prawej żyły biodrowej zewnętrznej i żyły udowej wspólnej
  • Zator gazowy mózgu

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Mechanizmy ciężkiego przebiegu choroby

Czynniki przyczyniające się do ciężkiego przebiegu zakażenia H1N1 obejmują:12

  • Nasilona odpowiedź zapalna – nadmierna aktywacja szlaków sygnałowych związanych z cytokinami i chemokinami, prowadząca do uszkodzenia tkanek
  • Zwiększona apoptoza – wirusa H1N1 może indukować nasiloną apoptozę komórek płuc, co przyczynia się do uszkodzenia tkanki płucnej
  • Zakażenia współistniejące – jednoczesne zakażenie innymi patogenami (np. bakteriami) może znacząco nasilić przebieg choroby

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Badania na modelach zwierzęcych wykazały, że współzakażenie wirusem H1N1 i Streptococcus suis serotyp 2 (SS2) prowadziło do znacznie cięższych objawów klinicznych, poważniejszych zmian patologicznych i nasilonej apoptozy w płucach w porównaniu do zakażeń pojedynczymi patogenami.1 Analiza mikromacierzy wykazała, że w przypadku współzakażenia regulacji ulegało znacznie więcej genów związanych z odpowiedzią immunologiczną, zapalną i apoptozą.1

Różnice między wirusem pandemicznym H1N1 a sezonowymi szczepami grypy

Wirus pandemiczny H1N1 z 2009 roku wykazywał kilka istotnych różnic w porównaniu do sezonowych szczepów grypy, co tłumaczy jego zdolność do wywołania globalnej pandemii.1

Różnice w patogenezie

W porównaniu do sezonowych szczepów grypy H1N1, wirus pandemiczny z 2009 roku wykazywał:12

  • Większą zjadliwość – powodował zwiększoną chorobowość u zakażonych osób
  • Szerszy tropizm tkankowy – replikował się nie tylko w jamie nosowej, ale również w tchawicy, oskrzelach i oskrzelikach
  • Wyższe miana wirusowe w tkance płucnej
  • Zdolność do replikacji w przewodzie pokarmowym

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Badania na modelach zwierzęcych wykazały, że wirus pandemiczny H1N1 z 2009 roku był bardziej patogenny niż sezonowy wirus grypy, z bardziej rozległą replikacją w układzie oddechowym.1

Różnice w odpowiedzi immunologicznej

Wirus pandemiczny H1N1 z 2009 roku wywoływał silniejszą odpowiedź immunologiczną w porównaniu do sezonowych szczepów grypy:12

  • Silniejsza aktywacja sygnałów wykrywających wirusa (receptory TLR, RLR i NLR)
  • Silniejsza aktywacja szlaków NF-κB i JAK-STAT
  • Wyższy poziom ekspresji większości cytokin i genów stymulowanych przez interferon

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Badania wykazały, że świński pochodzenia wirus H1N1 wywoływał silniejszą reakcję immunologiczną wrodzoną i stymulację prooksydacyjną, co może być ściśle związane ze zwiększoną patogennością.1

Różnice w transmisji

Pomimo zwiększonej zjadliwości, wirus pandemiczny H1N1 z 2009 roku wykazywał pewne różnice w transmisji w porównaniu do sezonowych szczepów grypy:1

  • Większe wydzielanie wirusa z górnych dróg oddechowych
  • Mniej efektywna transmisja drogą kropelkową w modelach zwierzęcych

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Zdolność wirusa pandemicznego H1N1 do szerszej replikacji w układzie oddechowym i wywoływania silniejszej odpowiedzi immunologicznej przyczyniła się do jego zwiększonej zjadliwości i zdolności do wywoływania ciężkiej choroby u niektórych osób.1

Znaczenie mechanizmów patogenezy dla terapii i profilaktyki

Zrozumienie patogenezy wirusa H1N1 ma kluczowe znaczenie dla opracowania skutecznych strategii leczenia i zapobiegania.1

Implikacje dla terapii

Leczenie zakażeń H1N1 opiera się głównie na:12

  • Lekach przeciwwirusowychoseltamiwir (Tamiflu) i zanamiwir (Relenza) hamują neuraminidazę wirusa, skracając czas trwania choroby i łagodząc objawy, szczególnie gdy są podawane we wczesnym stadium zakażenia
  • Leczeniu objawowym – odpoczynek, nawodnienie, lekka dieta, leki przeciwgorączkowe i przeciwbólowe
  • Antybiotykach – stosowanych w przypadku wtórnych infekcji bakteryjnych

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Zrozumienie roli szlaków aktywacji proteaz gospodarza, takich jak TMPRSS2, w aktywacji poprzez rozszczepienie hemaglutyniny wirusa, otwiera nowe możliwości terapeutyczne. Badania wykazały, że usunięcie genu Tmprss2 u myszy znacznie ograniczało rozprzestrzenianie się wirusa i patologię płuc po zakażeniu wirusem grypy A H1N1.1

Implikacje dla profilaktyki

Najskuteczniejszą metodą zapobiegania zakażeniom H1N1 jest szczepienie.1 Aktualnie wirus H1N1 jest uwzględniony w sezonowej szczepionce przeciw grypie.1

Zrozumienie mechanizmów adaptacji wirusa do człowieka może pomóc w opracowaniu lepszych szczepionek i identyfikacji nowych potencjalnych szczepów pandemicznych. Na przykład, odkrycie polimorfizmu SR w białku PB2 wirusa H1N1 z 2009, który zwiększa replikację wirusa w komórkach ludzkich, podkreśla znaczenie monitorowania zmian w genomie wirusów grypy.12

Badania wykazały również, że wcześniejsze zakażenie wirusem grypy A(H1N1)pdm09 może zapewnić pewien poziom ochrony krzyżowej przed innymi wirusami grypy, takimi jak wirus grypy A(H5N1) kladu 2.3.4.4.b, co ma znaczenie dla strategii szczepień i gotowości pandemicznej.12

Nadzór i gotowość pandemiczna

Zrozumienie pochodzenia i ewolucji wirusa pandemicznego H1N1 z 2009 roku podkreśla znaczenie:12

  • Globalnego nadzoru nad wirusami grypy u świń i innych zwierząt
  • Identyfikacji kluczowych adaptacji genetycznych, które umożliwiają wirusom przejście z gatunków zwierzęcych na człowieka
  • Opracowania skutecznych planów gotowości pandemicznej, obejmujących nadzór i usługi laboratoryjne, komunikację, utrzymanie usług społecznych, zapewnienie opieki medycznej oraz dostawy szczepionek i leków

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Szczególne znaczenie ma nadzór nad wirusami grypy u świń, które są ważnym rezerwuarem i miejscem reasortacji genetycznej wirusów grypy. Świnie są uważane za „naczynie mieszające” ze względu na obecność receptorów dla wirusów grypy zarówno ptasich, jak i ssaków, co zwiększa możliwość wymiany segmentów genetycznych i powstawania nowych, potencjalnie pandemicznych szczepów.12

Ciągły nadzór nad wirusami grypy zarówno u świń, jak i u ludzi jest absolutnie niezbędny, aby przewidzieć możliwe pojawienie się wirusów świńskiej grypy o potencjale pandemicznym i zapobiec kolejnej pandemii podobnej do tej z 2009 roku lub o gorszych konsekwencjach.1

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 H1N1 Influenza – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK513241/
    H1N1 influenza, a subtype of influenza A virus, is an infectious viral illness that causes both upper and, in some cases, lower respiratory tract infections in its host. […] A pandemic variant of H1N1, known as „swine flu,” emerged from the recombination of various prior swine, avian, and human influenza strains, causing a global pandemic affecting millions of people and impacting industries, including food and tourism. […] Swine influenza viruses can potentially infect humans if the antigenic characteristics of the virus change through the reassortment of different influenza strains. […] Such reassortments have led to pandemics, as seen in 1918 and 2009, when the virus acquired efficient person-to-person transmission capabilities. […] The H1N1 influenza virus belongs to the orthomyxovirus family and has a single-stranded negative-sense ribonucleic acid (RNA) genome.
  • #1 Influenza A virus subtype H1N1 – Wikipedia
    https://en.wikipedia.org/wiki/Influenza_A_virus_subtype_H1N1
    Influenza A virus subtype H1N1 (A/H1N1) is a subtype of influenza A virus (IAV). Some human-adapted strains of H1N1 are endemic in humans and are one cause of seasonal influenza (flu). Other strains of H1N1 are endemic in pigs (swine influenza) and in birds (avian influenza). Subtypes of IAV are defined by the combination of the antigenic H and N proteins in the viral envelope; for example, „H1N1” designates an IAV subtype that has a type-1 hemagglutinin (H) protein and a type-1 neuraminidase (N) protein. […] Under rare circumstances, one strain of the virus can acquire genetic material through genetic reassortment from a different strain and thus evolve to acquire new characteristics, enabling it to evade host immunity and occasionally to jump from one species of host to another. Major outbreaks of H1N1 strains in humans include the 1918 Spanish flu pandemic, the 1977 Russian flu pandemic and the 2009 swine flu pandemic, all of which were caused by strains of A(H1N1) virus which are believed to have undergone genetic reassortment.
  • #1 Influenza A virus subtype H1N1 – Wikipedia
    https://en.wikipedia.org/wiki/Influenza_A_virus_subtype_H1N1
    The 1918 flu caused an abnormally high number of deaths, possibly due to it provoking a cytokine storm in the body. After the 1918 flu infected lung cells, it frequently led to overstimulation of the immune system via release of immune response-stimulating cytokines (proteins that transmit signals between cells) into the lung tissue. This leads to extensive leukocyte migration towards the lungs, resulting in the destruction of lung cells and secretion of blood and mucus into the alveoli and airways. This makes it difficult for the patient to breathe and can result in suffocation. […] In the 2009 flu pandemic, the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses North American swine influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe „an unusually mongrelised mix of genetic sequences.” This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1.
  • #1 index : USDA ARS
    https://www.ars.usda.gov/oc/br/h1n1/index/
    Soon after the emergence of the H1N1 virus in April 2009, ARS scientists at the National Animal Disease Center in Ames, Iowa, began research using virus samples provided by the Centers for Disease Control and Prevention (CDC). […] ARS scientists at the Southeast Poultry Research Laboratory (SEPRL) quickly evaluated the pathogenesis of the new H1N1 virus in bird species to determine the potential risk to the poultry industry. […] Experts believe pigs can act as a „mixing vessel” for the reassortment of avian, swine and human influenza viruses, and might play an important role in the emergence of novel influenza viruses that could be capable of causing a human pandemic similar to the virus in the current outbreak. […] However, by the late 1990s, multiple strains and subtypes of triple reassortant swine influenza viruses-whose genomes include combinations of avian, human and swine influenza virus gene segments-had emerged and became predominant among North American pigs.
  • #1 Video | Top Medical Animation Studio – Scientific Animations
    http://swine-flu-h1n1-virus.scientificanimations.com/swine-flu-mechanism-of-action/
    Swine flu is a respiratory disease caused by a relatively new strain of influenza virus known as H1N1. […] Swine flu typically infects cells in the respiratory system first, such as the nose, throat or lungs. […] The H spike on the virus attaches to receptors on the surface of the healthy cell membrane. This allows the virus to penetrate the cell. […] The virus then travels towards the cells command center, the nucleus, and opens up to release its genetic content inside the cells cytoplasm. […] The viral genetic content enters the nucleus, where it uses the cells own machinery to print copies of itself. […] The viral blueprint causes ribosomes to manufacture proteins, like the H and N spikes, that are needed to create new virus molecules. […] In this way a single cell can produce millions of viruses. […] The viral load on the cell also causes the cell to burst. […] These newly generated viruses then go on to infect other healthy cells causing the flu.
  • #1 H1N1 Influenza – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK513241/
    Hemagglutinin triggers erythrocyte aggregation by binding to sialic acid and facilitates virus attachment to infected cells, enabling endocytosis. […] Subsequent fusion with the endosome, mediated by matrix proteins, allows viral RNA-dependent polymerase to initiate viral replication. […] Neuraminidase is crucial during viral budding by cleaving sialic receptors and promoting virus spread to neighboring cells. […] The known incubation period for the 2009 H1N1 influenza strains has a median duration of 2 days but ranges from 1 to 7 days. […] The virus replication occurs primarily in the upper and lower respiratory tract passages from the time of inoculation and peaks around 48 hours in most patients. […] The body’s immune reaction to the virus and the interferon response are the causes of the viral syndrome, which includes high fever, coryza, and myalgia.
  • #1 Influenza A Virus in Swine – Respiratory System – Merck Veterinary Manual
    https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-pigs/influenza-a-virus-in-swine
    Swine influenza is a highly contagious respiratory disease that results from infection with influenza A virus (IAV). […] The spectrum of IAV infection ranges from subclinical to acute. In the classic acute form, the virus multiplies in bronchial epithelium within 16 hours of infection and causes focal necrosis of the bronchial epithelium, focal atelectasis, and gross hyperemia of the lungs. […] Losses in reproduction associated with outbreaks appear to be secondary to the high fever response, because IAV very rarely causes systemic infection. […] A classic acute outbreak of IAV is characterized by sudden onset and rapid spread through the entire herd, often within 13 days. […] In uncomplicated infections, lesions are confined to the thoracic cavity. […] IAV is primarily diagnosed by detecting the influenza virus by RT-PCR, virus isolation, and occasionally by detecting antibodies against IAV in nonvaccinated animals. […] There is no effective treatment, although antimicrobials may reduce secondary bacterial infections and antipyretics may provide symptomatic relief.
  • #1 Pathogenesis and Transmission of Swine-Origin 2009 A(H1N1) Influenza Virus in Ferrets – ADS
    https://ui.adsabs.harvard.edu/abs/2009Sci…325..481M/abstract
    The swine-origin A(H1N1) influenza virus that has emerged in humans in early 2009 has raised concerns about pandemic developments. In a ferret pathogenesis and transmission model, the 2009 A(H1N1) influenza virus was found to be more pathogenic than a seasonal A(H1N1) virus, with more extensive virus replication occurring in the respiratory tract. […] Replication of seasonal A(H1N1) virus was confined to the nasal cavity of ferrets, but the 2009 A(H1N1) influenza virus also replicated in the trachea, bronchi, and bronchioles. […] Virus shedding was more abundant from the upper respiratory tract for 2009 A(H1N1) influenza virus as compared with seasonal virus, and transmission via aerosol or respiratory droplets was equally efficient. […] These data suggest that the 2009 A(H1N1) influenza virus has the ability to persist in the human population, potentially with more severe clinical consequences.
  • #1 Transmission and Pathogenesis of Swine-Origin 2009 A(H1N1) Influenza Viruses in Ferrets and Mice
    https://dspace.mit.edu/handle/1721.1/88974
    Recent reports of mild to severe influenza-like illness in humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better understand the pathogenesis and transmission of these viruses in mammals. […] In this study, selected 2009 A(H1N1) influenza isolates were assessed for their ability to cause disease in mice and ferrets and compared with a contemporary seasonal H1N1 virus for their ability to transmit to nave ferrets through respiratory droplets. […] In contrast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, replicated to higher titers in lung tissue, and were recovered from the intestinal tract of intranasally inoculated ferrets. […] The 2009 A(H1N1) influenza viruses exhibited less efficient respiratory droplet transmission in ferrets in comparison with the highly transmissible phenotype of a seasonal H1N1 virus. […] Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by characterizing the binding specificity of the viral hemagglutinin to the sialylated glycan receptors (in the human host) by use of dose-dependent direct receptor-binding and human lung tissue-binding assays.
  • #1 H1N1 Influenza – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK513241/
    The pathological findings associated with H1N1 influenza include multifocal destruction, potential desquamation of the pseudo-columnar and columnar epithelial cells, and possibly prominent hyperemia and edema in the submucosa. […] Histological changes in H1N1 influenza pneumonia include interstitial edema with possible inflammatory infiltrate, alveolar proteinaceous exudation associated with membrane formation, thrombosis of capillaries, necrosis of the alveolar septae, intra-alveolar hemorrhage, dislocation of desquamated pneumocytes with pyknotic nuclei into the surrounding alveolar spaces, diffuse alveolar damage with infiltration by the lymphocytes and histiocytes into the interstitium. […] The treatment of infected patients depends on the severity of symptoms of H1N1 influenza.
  • #1 H1 N1 influenza (swine flu) | PPT
    https://www.slideshare.net/slideshow/h1-n1-influenza-swine-flu/59771944
    Influenza viruses enter cells by receptor-mediated endocytosis, forming a virus-containing endosome. The viral hemagglutinin mediates fusion of the endosomal membrane with the virus envelope, and viral nucleocapsids are subsequently released into the cytoplasm. Pathogenesis and Immunity. Viral infection involves the ciliated columnar epithelial cells, but it may also involve other respiratory tract cells, including alveolar cells, mucous gland cells, and macrophages. In infected cells, virus replicates within 46 h, after which infectious virus is released to infect adjacent or nearby cells. The cells eventually become necrotic and desquamate; previously columnar epithelium is replaced by flattened and metaplastic epithelial cells. The host response to influenza infections involves a complex interplay of humoral antibody, local antibody, cell-mediated immunity, interferon, and other host defenses. Virus shedding generally stops within 25 days after symptoms first appear.
  • #1 Pathogenesis of Influenza A virus infection in swine – Articles – pig333, pig to pork community
    https://www.pig333.com/articles/pathogenesis-of-influenza-a-virus-infection-in-swine_9635/
    Once the virus is internalized by the cell, it replicates and many virus particles are released causing cell death or necrosis of the cell. […] The necrotic cells slough off into the lumen of the airway and inflammatory cells (mostly neutrophils) respond. […] Within 24 to 48 hours the hallmark microscopic lesion of necropurulent bronchiolitis can be seen. […] The remaining epithelial cells flatten out to cover the basement membrane (attenuation) and over the next 2-3 days the epithelial cells begin to multiply until they start to layer on top of each other (hyperplasia). […] Within 5-7 days, the virus has stopped replicating and the tissues begin to recover. […] In animals that have robust protection from their immune system provided by either a vaccine, previous infection or maternally-derived antibodies, the tissue damage caused by flu virus infection can be minimized.
  • #1
    https://pmc.ncbi.nlm.nih.gov/articles/PMC2863721/
    The pandemic H1N1 virus of 2009 (2009 H1N1) continues to cause illness worldwide, primarily in younger age groups. To better understand the pathogenesis of these viruses in mammals, we used a mouse model to evaluate the relative virulence of selected 2009 H1N1 viruses and compared them to a representative human triple-reassortant swine influenza virus that has circulated in pigs in the United States for over a decade preceding the current pandemic. […] All 2009 H1N1 viruses replicated efficiently in the lungs of mice and possessed a high degree of infectivity but did not cause lethal disease or exhibit extrapulmonary virus spread. […] Histologically, infection with the 2009 viruses resulted in lesions in the lung varying from mild to moderate bronchiolitis with occasional necrosis of bronchiolar epithelium and mild to moderate peribronchiolar alveolitis.
  • #1 H1 N1 influenza (swine flu) | PPT
    https://www.slideshare.net/slideshow/h1-n1-influenza-swine-flu/59771944
    A cytokine storm is the systemic expression of a healthy and vigorous immune system resulting in the release of more than 150 inflammatory mediators (cytokines, oxygen free radicals, and coagulation factors). Both pro-inflammatory cytokines (such as Tumor Necrosis Factor-alpha, InterLeukin-1, and InterLeukin-6) and anti-inflammatory cytokines (such as interleukin 10, and interleukin 1 receptor antagonist) are elevated in the serum, and the fierce and often lethal interplay of these cytokines is referred to as a „Cytokine Storm”. The primary contributors to the cytokine storm are TNF-a (Tumor Necrosis Factor-alpha) and IL-6 (Interleukin-6). The cytokine storm is an inappropriate (exaggerated) immune response that is caused by rapidly proliferating and highly activated T-cells or natural killer (NK) cells.
  • #1 Insights into the increasing virulence of the swine-origin pandemic H1N1/2009 influenza virus | Scientific Reports
    https://www.nature.com/articles/srep01601
    Pandemic H1N1/2009 viruses have been stabilized in swine herds and some strains display higher pathogenicity than the human-origin isolates. […] The transcriptome data show that Jia6/10 activates stronger virus-sensing signals, such as the toll-like receptor, RIG-I like receptor and NOD-like receptor signalings, as well as a stronger NF-B and JAK-STAT signals, which play significant roles in inducing innate immunity. […] Most cytokines and interferon-stimulated genes show higher expression level in Jia6/10 infected groups. […] Collectively, our data reveal that the swine-origin pandemic H1N1/2009 virus elicits a stronger innate immune reaction and pro-oxidation stimulation, which might relate closely to the increasing pathogenicity. […] In the present study, we showed that the swine-origin H1N1/2009 virus displayed higher pathogenicity than the human-origin H1N1/2009 virus including more severe body weight loss and pathological lung damage as well as higher cytokine expression in infected mouse model.
  • #1 Insights into the increasing virulence of the swine-origin pandemic H1N1/2009 influenza virus | Scientific Reports
    https://www.nature.com/articles/srep01601
    Furthermore, the Jia6/10 virus stimulated higher expression of IL1, IL6 and TNF, indicating that this virus elicited a stronger innate immune reaction in infected mouse lung tissues than LN/09 did. […] The innate immune system is the first defense of an organism and is associated with a highly conserved host-cell signaling mechanism that protects the host against invading pathogens. […] Generally, the Jia6/10 virus activated stronger TLR, RLR and NLR signaling reactions than LN/09, which might be associated with the higher pathogenicity of Jia6/10. […] The data revealed that the important pro-inflammatory factor genes (IL1b and IL6) increased significantly in both virus-infected groups and the expression values were obviously higher on day 3 than day 5. […] Notably, the expression of most cytokines and chemokines was higher in the Jia6/10-infected mouse lungs than in the LN/09-infected groups, which indicated that Jia6/10 activated a much stronger inflammatory response and greater inflammatory cell recruitment. […] The high mutation rate of the Jia6/10 genome might relate to the stronger pro-oxidation reaction elicited by the Jia6/10 virus and may partially verify the role of ROS in the promotion of genome mutation.
  • #1 Pathogenesis and transmission of the novel swine-origin influenza virus A/H1N1 after experimental infection of pigs | Microbiology Society
    https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.014480-0?crawler=true
    Influenza virus A/H1N1, which is currently causing a pandemic, contains gene segments with ancestors in the North American and Eurasian swine lineages. […] To get insights into virus replication dynamics, clinical symptoms and virus transmission in pigs, we infected animals intranasally with influenza virus A/Regensburg/D6/09/H1N1. […] Virus excretion in the inoculated pigs was detected in nasal swabs from 1 day post-infection (p.i.) onwards and the pigs developed generally mild symptoms, including fever, sneezing, nasal discharge and diarrhoea. […] Contact pigs became infected, shed virus and developed clinical symptoms similar to those in the inoculated animals. […] Plasma samples of all animals remained negative for virus RNA. […] Nucleoprotein- and haemagglutinin H1-specific antibodies could be detected by ELISA 7 days p.i. […] CD4+ T cells became activated immediately after infection and both CD4+ and CD8+ T-cell populations expanded from 3 to 7 days p.i., coinciding with clinical signs. […] Contact chickens remained uninfected, as judged by the absence of virus excretion, clinical signs and seroconversion.
  • #1 New Biological Route for Swine Flu to Human Infections – Berkeley Lab – Berkeley Lab News Center
    https://newscenter.lbl.gov/2009/12/09/swine-flu-to-human/
    Berkeley Lab researchers have discovered a new biological pathway by which the H1N1 flu virus can make the jump from swine to humans. Early tests indicate this pathway may have played an important role in transmitting the virus into humans. […] Early test results indicate that a heretofore unknown mutation in one of the H1N1 genes may have played an important role in transmitting the virus into humans. […] We have identified an adaptive mutation in the swine origin H1N1 influenza A virus a pair of amino acid variants termed the SR polymorphism that enhance replication, and potentially pathogenesis of the virus in humans. […] A mutation in the H1N1 influenza A virus – a pair of amino acid variants termed the SR polymorphism was found to enhance replication of the virus in humans. […] One way in which an influenza virus surmounts biological barriers to cross-species infection is through a mutational change in its polymerase, the enzyme that enables the virus to replicate.
  • #1 Conference 02 – 2014  &nbsp Case: 02     &nbsp 20140910
    https://www.askjpc.org/wsco/wsc_showcase2.php?id=ZVdRTjBwRjR0TllPOGVzdWJlVmQ4Zz09
    Influenza is an orthomyxovirus, a single-stranded RNA virus which is well known for its ability to constantly adapt through spontaneous mutations of its hemaglutinin and neuraminidase proteins (antigenic drift) or via recombination of genes with those in strains infecting other species (antigenic shift). […] Newly reassorted viruses pose a significant biosecurity and management problem for the swine industry, with the need for protection against the increasingly antigenically diverse viruses being of significant concern. […] In addition to hemagglutinin (used for attachment to and internalization of host cells) and neuraminidase (which prevents viral progeny aggregation), the proteins that influenza is classified by, there are several others important for disease pathogenesis and diagnostics.
  • #1 Genetic characterization and pathogenicity of a Eurasian avian-like H1N1 swine influenza reassortant virus | Virology Journal | Full Text
    https://virologyj.biomedcentral.com/articles/10.1186/s12985-022-01936-6
    Swine influenza viruses (SIV), considered the mixing vessels of influenza viruses, posed a significant threat to global health systems and are dangerous pathogens. Eurasian avian-like H1N1(EA-H1N1) viruses have become predominant in swine populations in China since 2016. […] The SIV(A/swine/Heilongjiang/GN/2020) with hemagglutination activity was isolated from lung samples and was successfully identified by RT-PCR, IFA, WB and TEM. […] Pathogenicity in mice showed that the EA-H1N1 could cause lethal or exhibit extrapulmonary virus spread and cause severe damage to respiratory tracts effectively proliferating in lung and trachea. […] These data suggest that A/swine/Heilongjiang/GN/2020 (EA-H1N1) had high pathogenicity and could be systemic spread in mice. […] The virus retained configurations (SA2,6Gal) in HA1 (position Q223 and G225), predicting that it had an affinity for mammalian by receptor-binding. Pathogenicity in mice showed that A/swine/Heilongjiang/GN/2020 could cause lethal or exhibit extrapulmonary virus spread and cause severe damage to respiratory tracts effectively proliferating in lungs and tracheas.
  • #1 Swine Influenza – Swine Diseases
    https://open.lib.umn.edu/swinedisease/chapter/swine-influenza/
    Swine Influenza Virus (SIV) is one of the leading causes of severe respiratory diseases in pigs. Out of the 3 types (A, B, and C), only influenza A creates issues in swine. That being said, there are many strains of the virus, subtyped by the nature of hemagglutinin (H or HA) and neuraminidase (N or NA) glycoproteins on the surface of the viral envelope. The influenza genome is made of 8 RNA segments, making it highly variable due to antigenic drift and antigenic shifts. […] Antigenic shift: Mechanism by which two (or more) virus strains create a brand new strain by co-infecting a cell and exchanging entire segments of genetic material (H and/or N in the case of influenza). This new strain then possesses completely new antigens, making the population naive to it. Antigenic drift: Mechanism for variation in viruses that involves the accumulation of mutations within the genes that code for antibody-binding sites. This results in a new strain of virus particles which cannot be inhibited as effectively by the antibodies that were originally targeted against previous strains, making it easier for the virus to spread throughout a partially immune population.
  • #1 Swine Flu (H1N1): What Is It, Causes, Treatments & Prevention
    https://my.clevelandclinic.org/health/diseases/23928-swine-flu-h1n1
    Swine flu (H1N1) is an infection that a type of flu (influenza) virus causes. Its called swine flu because its similar to a flu virus that affects pigs (swine). The virus leads to a lung (respiratory) disease in pigs. Swine flu (H1N1) is a respiratory infection in humans. […] A virus causes swine flu (H1N1). It spreads from person to person. When a person coughs or sneezes, droplets go into the air. You can get the infection when you breathe in (inhale) the virus. You can also get the infection when you touch a contaminated surface and then touch your mouth, nose or eyes. […] Swine flu (H1N1) is contagious. It can spread from person to person. […] Most people with swine flu (H1N1) who are otherwise healthy dont need special drugs or treatments. If you have swine flu, you should get plenty of rest, drink fluids, eat a light diet, stay home, and take acetaminophen (Tylenol) to reduce fever and relieve aches and pains.
  • #1 H1N1 flu (swine flu) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/swine-flu/symptoms-causes/syc-20378103
    The H1N1 flu, sometimes called swine flu, is a type of influenza A virus. […] During the 2009-10 flu season, a new H1N1 virus began causing illness in humans. It was often called swine flu and was a new combination of influenza viruses that infect pigs, birds and humans. […] Influenza viruses such as H1N1 infect the cells that line your nose, throat and lungs. The virus spreads through the air in droplets released when someone with the virus coughs, sneezes, breathes or talks. The virus enters your body when you breathe in contaminated droplets. […] People with the virus are likely able to spread the virus from about a day before symptoms appear until about four days after they start. […] Factors that may increase your risk of developing H1N1 or other influenza viruses or their complications include: […] Influenza complications include: […] The H1N1 virus is included in the seasonal flu vaccine. […] The flu vaccine can lower your risk of getting the flu. It also can lower the risk of having serious illness from the flu and needing to stay in the hospital.
  • #1 Influenza A virus subtype H1N1 – Wikipedia
    https://en.wikipedia.org/wiki/Influenza_A_virus_subtype_H1N1
    A study conducted in coordination with the University of Michigan Health Service scheduled for publication in the December 2009 American Journal of Roentgenology warned that H1N1 flu can cause pulmonary embolism, surmised as a leading cause of death in this pandemic. The study authors suggest physician evaluation via contrast enhanced CT scans for the presence of pulmonary emboli when caring for patients diagnosed with respiratory complications from a „severe” case of the H1N1 flu. H1N1 may induce other embolic events, such as myocardial infarction, bilateral massive DVT, arterial thrombus of infrarenal aorta, thrombosis of right external iliac vein and common femoral vein or cerebral gas embolism. The type of embolic events caused by H1N1 infection are summarized in a 2010 review by Dimitroulis Ioannis et al.
  • #1 Swine Flu (H1N!): Pandemic, Vaccine, Causes, Symptoms, Treatment & Contagious
    https://www.medicinenet.com/swine_flu/article.htm
    Second, pigs can play a unique role as an intermediary host to new flu types because pig respiratory cells can be infected directly with bird, human, and other mammalian flu viruses. […] Symptoms of swine flu are similar to most influenza infections: fever (100 F or greater), cough (usually dry), nasal secretions, fatigue, and headache, with fatigue being reported in most infected individuals. […] Death often occurs from secondary bacterial infection of the lungs; appropriate antibiotics need to be used in these patients. […] The most serious complication of the flu is pneumonia. […] The best treatment for influenza infections in humans is prevention by vaccination. […] Several antiviral agents have been reported to help prevent or reduce the effects of swine flu. […] The flu shot (vaccine) is made from killed virus particles so a person cannot get the flu from a flu shot.
  • #1 H1N1 Influenza (Swine Flu): Practice Essentials, Background, Epidemiology
    https://emedicine.medscape.com/article/1807048-overview
    The ability to trace outbreaks of swine flu in humans dates back to investigation of the 1918 Spanish influenza pandemic, which infected one third of the worlds population (an estimated 500 million people) and caused approximately 50 million deaths. […] In humans, the severity of swine influenza can vary from mild to severe. […] Treatment largely is supportive and consists of bedrest, increased fluid consumption, cough suppressants, and antipyretics and analgesics (eg, acetaminophen, nonsteroidal anti-inflammatory drugs) for fever and myalgias. Severe cases may require intravenous hydration and other supportive measures. Antiviral agents may also be considered for treatment or prophylaxis. […] A review of medical records from the 2009 US pandemic found hospitalized patients with pandemic H1N1 and pneumonia were at risk for severe outcomes including ARDS, sepsis, and death. However, patients often received delayed antiviral treatment (2 days after illness onset). Patients with H1N1 and pneumonia should receive early and aggressive treatment with antibiotics and influenza antiviral agents. […] In a multicenter study in Britain consisting of over 1500 patients, independent predictors of severe outcome included age 55 to 64 years, certain chronic lung diseases, underlying neurological disease, obesity, delayed admission (5 days after illness onset), pneumonia, and others.
  • #1 Investigation of Pathogenesis of H1N1 Influenza Virus and Swine Streptococcus suis Serotype 2 Co-Infection in Pigs by Microarray Analysis | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124086
    Pathway analysis indicated that the cytokine-cytokine receptor interactions, MAPK, toll-like receptor, complement and coagulation cascades, antigen processing and presentation, and apoptosis pathway were significantly regulated in the co-infected group. […] This observation suggested that a certain level of synergy was induced by H1N1 and SS2 co-infection with significantly stronger inflammatory and apoptosis responses, which may lead to more serious respiratory disease syndrome and pulmonary pathological lesion. […] Stronger inflammatory and apoptosis responses were determined to be important contributors to the increased pathogenicity caused by swine H1N1 and SS2 co-infection. […] The clinical and pathological findings demonstrated that H1N1 and SS2 co-infection enhanced the virulence in pigs. In addition, the transcriptional profiles indicated that co-infection resulted in augmented inflammatory and apoptosis responses, which could account for the increased pathogenicity.
  • #1 Investigation of Pathogenesis of H1N1 Influenza Virus and Swine Streptococcus suis Serotype 2 Co-Infection in Pigs by Microarray Analysis | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124086
    Swine influenza virus and Streptococcus suis are two important contributors to the porcine respiratory disease complex, and both have significant economic impacts. […] However, the co-infection pathogenesis in pigs is unclear. In the present study, co-infection experiments were performed using swine H1N1 influenza virus and Streptococcus suis serotype 2 (SS2). The H1N1-SS2 co-infected pigs exhibited more severe clinical symptoms, serious pathological changes, and robust apoptosis of lungs at 6 days post-infection compared with separate H1N1 and SS2 infections. […] Results showed 457, 411, and 844 differentially expressed genes in the H1N1, SS2, and H1N1-SS2 groups, respectively, compared with the control. Noticeably, genes associated with the immune, inflammatory, and apoptosis responses were highly overexpressed in the co-infected group.
  • #1 2009 H1N1 Pandemic (H1N1pdm09 virus) | Pandemic Influenza (Flu) | CDC
    https://archive.cdc.gov/www_cdc_gov/flu/pandemic-resources/2009-h1n1-pandemic.html
    The (H1N1)pdm09 virus was very different from H1N1 viruses that were circulating at the time of the pandemic. […] It is estimated that 0.001 percent to 0.007 percent of the worlds population died of respiratory complications associated with (H1N1)pdm09 virus infection during the first 12 months the virus circulated. […] Cytokine and Chemokine Profiles in Lung Tissues from Fatal Cases of 2009 Pandemic Influenza A (H1N1): Role of the Host Immune Response in Pathogenesis. […] Transmission and Pathogenesis of Swine-Origin 2009 A(H1N1) Influenza Viruses in Ferrets and Mice.
  • #1 Tmprss2 Is Essential for Influenza H1N1 Virus Pathogenesis in Mice | PLOS Pathogens
    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003774
    Tmprss2 is essential for spread and pathogenesis of H1N1 influenza viruses in mice. […] The cleavage activation of the influenza virus hemagglutinin (HA) by host cell proteases is essential for viral infectivity. […] Here, we show that deletion of a single HA-activating protease gene, Tmprss2, in mice inhibits spread of mono-basic H1N1 influenza viruses, including the pandemic 2009 swine influenza virus. […] In conclusion, these results identify TMPRSS2 as a host cell factor essential for viral spread and pathogenesis of mono-basic H1N1 and H3N2 influenza A viruses. […] Our study shows that deletion of Tmprss2 in knock-out mice strongly limits virus spread and lung pathology after H1N1 influenza A virus infection. […] Thus, the absence of TMPRSS2 largely protects animals from virus spread and virus induced pathogenesis.
  • #1 Swine Flu (H1N1): What Is It, Causes, Treatments & Prevention
    https://my.clevelandclinic.org/health/diseases/23928-swine-flu-h1n1
    If youre very ill, your healthcare provider may prescribe an antiviral medicine. Antiviral drugs such as oseltamivir (Tamiflu) or zanamivir (Relenza) can kill the virus. These drugs can shorten the time youre sick and help ease your symptoms. Antiviral drugs work best if you start taking them when your symptoms begin. […] Swine flu (H1N1) once caused a serious worldwide pandemic. The virus is under control today, but people can and do still get very sick from H1N1. If you do get sick, make sure to get plenty of rest, drink fluids and call your healthcare provider if symptoms worsen.
  • #1 H1N1 influenza (Swine flu) – UF Health
    https://ufhealth.org/conditions-and-treatments/h1n1-influenza-swine-flu
    The H1N1 virus (swine flu) is an infection of the nose, throat, and lungs. It is caused by the H1N1 influenza virus. […] Earlier forms of the H1N1 virus were found in pigs (swine). Over time, the virus changed (mutated) and infected humans. H1N1 is a new virus first detected in humans in 2009. It spread quickly around the world. […] The H1N1 virus is now considered a regular flu virus. It is one of the three viruses included in the regular (seasonal) flu vaccine.
  • #1 Effect of Prior Influenza A(H1N1)pdm09 Virus Infection on Pathogenesis and Transmission of Human Influenza A(H5N1) Clade 2.3.4.4b Virus in Ferret Model – Volume 31, Number 3—March 2025 – Emerging Infectious Diseases journal – CDC
    https://wwwnc.cdc.gov/eid/article/31/3/24-1489_article
    Reports of human infections with influenza A(H5N1) clade 2.3.4.4b viruses associated with outbreaks in dairy cows in the United States underscore the need to assess the potential cross-protection conferred by existing influenza immunity. […] Our results showed that prior influenza A(H1N1)pdm09 virus infection more effectively reduced the replication and transmission of the H5N1 virus than did the H7N9 virus, a finding supported by the presence of group 1 hemagglutinin stalk and N1 neuraminidase antibodies in preimmune ferrets. […] Our findings suggest that prior influenza A(H1N1)pdm09 virus infection may confer some level of protection against influenza A(H5N1) clade 2.3.4.4.b virus. […] We showed that ferrets with existing pH1N1 virus immunity had reduced disease severity and limited viral systemic spread after aerosol inhalation exposure to Texas/37 virus.
  • #1 Researchers Discover the 2009 Swine Flu Pandemic Originated in Mexico | Mount Sinai – New York
    https://www.mountsinai.org/about/newsroom/2016/researchers-discover-the-2009-swine-flu-pandemic-originated-in-mexico
    The 2009 swine H1N1 flu pandemic — responsible for more than 17,000 deaths worldwide — originated in pigs from a very small region in central Mexico, a research team headed by investigators at the Icahn School of Medicine at Mount Sinai is reporting. […] Researchers used state-of-the-art genetic analysis to identify the precise location and the main molecular transformations that allowed a pig influenza virus to jump into humans. […] Knowing where and how an animal influenza virus infects humans and spreads all over the world helps us understand how we can reduce risk of these pandemics, says the study’s senior author, Adolfo García-Sastre, PhD, Director of the Global Health and Emerging Pathogens Institute, Irene and Dr. Arthur M. Fishberg Chair and Professor of Medicine (Infectious Diseases), and Professor of Microbiology at the Icahn School of Medicine at Mount Sinai.
  • #1 RRH: Rural and Remote Health article: 1262 – Swine influenza (H1N1) pandemic: developing countries’ perspective
    https://www.rrh.org.au/journal/article/1262/
    Control of the pandemic (H1N1) 2009 is dependent on comprehensive approaches taken by staff of local departments of health, veterinary sciences and animal husbandry. […] The WHO urges all countries to develop and implement national pandemic preparedness plans to prevent, mitigate and minimize the effects of the pandemic (H1N1) 2009. […] Effective plans for combating any catastrophic infectious disease (such as pandemic influenza) address five issues: (i) surveillance and laboratory services; (ii) communications; (iii) maintenance of community services; (iv) providing medical care; and (v) the supply and delivery of vaccines and drugs. […] There is every reason for attention to appropriate pandemic preparedness plans in each developing country to prevent, mitigate and recover from this potentially dangerous strain of influenza.
  • #1 Swine flu lineage has passed from humans to pigs 400 times
    https://sciencemediacentre.es/en/reactions-lineage-so-called-swine-flu-has-passed-humans-pigs-almost-400-times-2009
    It is well known that the pig is a key species in the emergence of zoonotic influenza viruses. In fact, it is considered the main shaker species, since it is susceptible to swine, human and bird flu viruses. […] Since the start of the H1N1 influenza A (pdm2009) pandemic, numerous cases of transmission of this pandemic virus from humans to pigs (reverse zoonosis) have been documented in Europe and the USA. […] The introduction and establishment of new viruses of human origin in pigs increases the heterogeneity of the viruses in this species and increases the chances of the origin of swine flu strains capable of inverse transmission to humans and causing new pandemics. […] This evolutionary closeness between swine and human influenza viruses explains the relative ease of reciprocal transmission of viruses between the two species. For this reason, close and constant surveillance of influenza viruses in both species is absolutely necessary to anticipate possible emergencies of swine flu viruses with pandemic potential and the reissue of another pandemic similar to or with worse consequences than the one suffered in 2009.
  • #2 H1N1 flu (swine flu) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/swine-flu/symptoms-causes/syc-20378103
    The H1N1 flu, sometimes called swine flu, is a type of influenza A virus. […] During the 2009-10 flu season, a new H1N1 virus began causing illness in humans. It was often called swine flu and was a new combination of influenza viruses that infect pigs, birds and humans. […] Influenza viruses such as H1N1 infect the cells that line your nose, throat and lungs. The virus spreads through the air in droplets released when someone with the virus coughs, sneezes, breathes or talks. The virus enters your body when you breathe in contaminated droplets. […] People with the virus are likely able to spread the virus from about a day before symptoms appear until about four days after they start. […] Factors that may increase your risk of developing H1N1 or other influenza viruses or their complications include: […] Influenza complications include: […] The H1N1 virus is included in the seasonal flu vaccine. […] The flu vaccine can lower your risk of getting the flu. It also can lower the risk of having serious illness from the flu and needing to stay in the hospital.
  • #2 index : USDA ARS
    https://www.ars.usda.gov/oc/br/h1n1/index/
    The genetic makeup of swine influenza viruses is identical to other influenza A viruses and consists of 8 segments of RNA that code for different proteins. […] These glycoproteins also determine the host range, antigenicity and the pathogenicity of the viruses. […] Pigs have long been considered a potential source for new and novel influenza viruses that infect humans, as they have receptors on their cells that bind both mammalian and avian influenza viruses, increasing the opportunity for the exchange of genetic segments of the virus. […] Identification and characterization of a highly virulent triple reassortant H1N1 swine influenza virus in the United States. […] Pathogenicity and transmission in pigs of the novel A(pN2)v influenza virus isolated from humans and characterization of swine pN2 viruses isolated in 2010-2011. […] Swine influenza matrix 2 (M2) protein contributes to protection against infection with different H1 swine influenza virus (SIV) isolates.
  • #2 2009 swine flu pandemic originated in Mexico, researchers discover | ScienceDaily
    https://www.sciencedaily.com/releases/2016/06/160627160935.htm
    The scientists say their findings represent the first time that the origin of an influenza pandemic virus has been determined in such detail. […] Researchers used state-of-the-art genetic analysis to identify the precise location and the main molecular transformations that allowed a pig influenza virus to jump into humans. […] Determining the original location of the 2009 swine flu, known as an A/H1N1 pathogen, lends a note of caution to evolving efforts to track problematic animal and bird viruses, Dr. Garcia-Sastre says. […] The 2009 A/H1N1 was also a derivative of two different strains of swine influenza — one that had been circulating in Europe and Asia and another that was circulating in the Americas, especially North America. […] The 2009 swine virus was therefore a „quadruple” reassortment, Dr. Garcia-Sastre says.
  • #2 Swine Influenza – Swine Diseases
    https://open.lib.umn.edu/swinedisease/chapter/swine-influenza/
    The swine species is critical in the control of influenza because it is a great recombinant species. Indeed, pigs can replicate both human and avian strains in addition to the swine ones, promoting reassortments. […] Three main subtypes are seen today in the US, H1N1, H1N2 and H3N2. Several strains are of interest to understand the evolution of influenza genome over the years. The oldest flu strain dates back to the 1910s and is still called the Classical North American H1N1. Originating from a human virus, the Classical H1N1 gene segments can still be found in H1N1 strains today. Similarly, seasonal H3N2 strains can be found in swine from the human one, which was identified in 1968. Those 2 strains (H1N1 and H3N2) reasorted with some avian influenza viruses to create in 1998, the triple reassortant H1N2. This strain is very specific from North America. Finally, in 2009, an Asian strain of H1N1 reassorted with the Triple H1N2 to create the pandemic H1N1 virus. Obviously, this figure shows the major genetic changes, the antigenic shift; it is important to remember that many more changes occur to the genome in the form of antigenic drift.
  • #2 H1N1 Influenza – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK513241/
    Hemagglutinin triggers erythrocyte aggregation by binding to sialic acid and facilitates virus attachment to infected cells, enabling endocytosis. […] Subsequent fusion with the endosome, mediated by matrix proteins, allows viral RNA-dependent polymerase to initiate viral replication. […] Neuraminidase is crucial during viral budding by cleaving sialic receptors and promoting virus spread to neighboring cells. […] The known incubation period for the 2009 H1N1 influenza strains has a median duration of 2 days but ranges from 1 to 7 days. […] The virus replication occurs primarily in the upper and lower respiratory tract passages from the time of inoculation and peaks around 48 hours in most patients. […] The body’s immune reaction to the virus and the interferon response are the causes of the viral syndrome, which includes high fever, coryza, and myalgia.
  • #2 H1 N1 influenza (swine flu) | PPT
    https://www.slideshare.net/slideshow/h1-n1-influenza-swine-flu/59771944
    Influenza viruses enter cells by receptor-mediated endocytosis, forming a virus-containing endosome. The viral hemagglutinin mediates fusion of the endosomal membrane with the virus envelope, and viral nucleocapsids are subsequently released into the cytoplasm. Pathogenesis and Immunity. Viral infection involves the ciliated columnar epithelial cells, but it may also involve other respiratory tract cells, including alveolar cells, mucous gland cells, and macrophages. In infected cells, virus replicates within 46 h, after which infectious virus is released to infect adjacent or nearby cells. The cells eventually become necrotic and desquamate; previously columnar epithelium is replaced by flattened and metaplastic epithelial cells. The host response to influenza infections involves a complex interplay of humoral antibody, local antibody, cell-mediated immunity, interferon, and other host defenses. Virus shedding generally stops within 25 days after symptoms first appear.
  • #2 Pathogenesis of Influenza A virus infection in swine – Articles – pig333, pig to pork community
    https://www.pig333.com/articles/pathogenesis-of-influenza-a-virus-infection-in-swine_9635/
    Once the virus is internalized by the cell, it replicates and many virus particles are released causing cell death or necrosis of the cell. […] The necrotic cells slough off into the lumen of the airway and inflammatory cells (mostly neutrophils) respond. […] Within 24 to 48 hours the hallmark microscopic lesion of necropurulent bronchiolitis can be seen. […] The remaining epithelial cells flatten out to cover the basement membrane (attenuation) and over the next 2-3 days the epithelial cells begin to multiply until they start to layer on top of each other (hyperplasia). […] Within 5-7 days, the virus has stopped replicating and the tissues begin to recover. […] In animals that have robust protection from their immune system provided by either a vaccine, previous infection or maternally-derived antibodies, the tissue damage caused by flu virus infection can be minimized.
  • #2 Localization and immunohistochemical detection of swine influenza A virus subtype H1N1 antigen in formalin-fixed, paraffin-embedded lung tissues from naturally infected pigs | Beni-Suef University Journal of Basic and Applied Sciences | Full Text
    https://bjbas.springeropen.com/articles/10.1186/s43088-020-0039-3
    In the present study, histopathology revealed suppurative bronchitis, bronchiolitis, and pneumonia with concurrent epithelial hyperplasia with or without widespread degeneration and necrosis of the infected epithelial cells and thickening of alveolar septa due to cellular infiltration consisting predominantly of neutrophils and lymphocytes with a few macrophages and plasma cells. […] SIV has been reported to have a tropism for the respiratory system where it attaches to and replicates in epithelial cells of the upper respiratory tract. […] The present result demonstrated that SIV antigens can be detected in formalin-fixed, paraffin-embedded tissue specimens of the pig using a monoclonal antibody. […] The immunohistochemical findings of the present study are consistent with the results of the previous studies in terms of distribution and localization of the viral antigens in the lungs.
  • #2
    https://pmc.ncbi.nlm.nih.gov/articles/PMC2863721/
    The pandemic H1N1 virus of 2009 (2009 H1N1) continues to cause illness worldwide, primarily in younger age groups. To better understand the pathogenesis of these viruses in mammals, we used a mouse model to evaluate the relative virulence of selected 2009 H1N1 viruses and compared them to a representative human triple-reassortant swine influenza virus that has circulated in pigs in the United States for over a decade preceding the current pandemic. […] All 2009 H1N1 viruses replicated efficiently in the lungs of mice and possessed a high degree of infectivity but did not cause lethal disease or exhibit extrapulmonary virus spread. […] Histologically, infection with the 2009 viruses resulted in lesions in the lung varying from mild to moderate bronchiolitis with occasional necrosis of bronchiolar epithelium and mild to moderate peribronchiolar alveolitis.
  • #2
    https://pmc.ncbi.nlm.nih.gov/articles/PMC2863721/
    Taken together, these studies demonstrate that the 2009 H1N1 viruses exhibited mild to moderate virulence in mice compared with highly pathogenic viruses. […] The 2009 H1N1 viruses did not mount lethal infections in mice (LD50, 106 EID50 or PFU), and with the exception of Mex/4482 virus, which caused 19% weight loss at the height of infection, morbidity was mild with 10% transient loss of initial body weight. […] In contrast to all 2009 H1N1 viruses tested, which were highly infectious but not lethal in the mouse, the reconstructed 1918 H1N1 virus and the highly pathogenic avian influenza (HPAI) H5N1 virus VN/1203 demonstrated enhanced morbidity and mortality in this model. […] The most severe lesions observed (mean histological lesion score, 3.2 to 3.3) were with VN/1203 and 1918 viruses, which produced mild to severe necrosis of bronchiolar epithelium with neutrophilic inflammation and peribronchiolar to diffuse neutrophilic alveolitis with necrosis of alveolar epithelium and prominent alveolar to interlobular edema at the hilum.
  • #2 Insights into the increasing virulence of the swine-origin pandemic H1N1/2009 influenza virus | Scientific Reports
    https://www.nature.com/articles/srep01601
    Given that the swine-origin pandemic H1N1/2009 viruses had displayed distinct biological properties and some of them displayed increased virulence as well as the potential for reverse swine-to-human transmission, we chose LN/09 and Jia6/10 to investigate the different pathogenesis and further to study the mechanism involving in the interaction between the human- and novel swine-origin H1N1/2009 isolates and their host. […] The Jia6/10 virus caused more significant body weight loss and four (50%) deaths of the infected mice. […] However, the body weight of the mice infected by LN/09 virus only displayed slight loss up to day 6 and then maintained increase. […] Meanwhile, the mice infected by Jia6/10 developed more severe pathological damage, including necrosis of the alveolar epithelial cells, edema and interstitium broadening as well as infiltration of the inflammatory cells.
  • #2 Insights into the increasing virulence of the swine-origin pandemic H1N1/2009 influenza virus | Scientific Reports
    https://www.nature.com/articles/srep01601
    Furthermore, the Jia6/10 virus stimulated higher expression of IL1, IL6 and TNF, indicating that this virus elicited a stronger innate immune reaction in infected mouse lung tissues than LN/09 did. […] The innate immune system is the first defense of an organism and is associated with a highly conserved host-cell signaling mechanism that protects the host against invading pathogens. […] Generally, the Jia6/10 virus activated stronger TLR, RLR and NLR signaling reactions than LN/09, which might be associated with the higher pathogenicity of Jia6/10. […] The data revealed that the important pro-inflammatory factor genes (IL1b and IL6) increased significantly in both virus-infected groups and the expression values were obviously higher on day 3 than day 5. […] Notably, the expression of most cytokines and chemokines was higher in the Jia6/10-infected mouse lungs than in the LN/09-infected groups, which indicated that Jia6/10 activated a much stronger inflammatory response and greater inflammatory cell recruitment. […] The high mutation rate of the Jia6/10 genome might relate to the stronger pro-oxidation reaction elicited by the Jia6/10 virus and may partially verify the role of ROS in the promotion of genome mutation.
  • #2 New Biological Route for Swine Flu to Human Infections – Berkeley Lab – Berkeley Lab News Center
    https://newscenter.lbl.gov/2009/12/09/swine-flu-to-human/
    Berkeley Lab researchers have discovered a new biological pathway by which the H1N1 flu virus can make the jump from swine to humans. Early tests indicate this pathway may have played an important role in transmitting the virus into humans. […] Early test results indicate that a heretofore unknown mutation in one of the H1N1 genes may have played an important role in transmitting the virus into humans. […] We have identified an adaptive mutation in the swine origin H1N1 influenza A virus a pair of amino acid variants termed the SR polymorphism that enhance replication, and potentially pathogenesis of the virus in humans. […] A mutation in the H1N1 influenza A virus – a pair of amino acid variants termed the SR polymorphism was found to enhance replication of the virus in humans. […] One way in which an influenza virus surmounts biological barriers to cross-species infection is through a mutational change in its polymerase, the enzyme that enables the virus to replicate.
  • #2 New Biological Route for Swine Flu to Human Infections – Berkeley Lab – Berkeley Lab News Center
    https://newscenter.lbl.gov/2009/12/09/swine-flu-to-human/
    The processes regulating emergence of viruses into the human population involve a complex interplay between virus and host, Doudna says, and understanding the mechanisms by which influenza viruses acquire the ability to infect multiple species is imperative to controlling future outbreaks. […] The SR polymorphism mutation in PB2 accomplishes the same goal as the change from glutamic acid to lysine, Mehle explains. The fact that all of the 2009 H1N1 isolates contain this second mutation supports the notion that it is important for transmission into humans, although we dont yet know the relative importance of the changes in the polymerase versus mutations elsewhere in the virus.
  • #2 Conference 02 – 2014  &nbsp Case: 02     &nbsp 20140910
    https://www.askjpc.org/wsco/wsc_showcase2.php?id=ZVdRTjBwRjR0TllPOGVzdWJlVmQ4Zz09
    The polymerase PB2 directs cell processes toward virus replication and is considered most significant of the polymerases with regard to pathogenicity. […] The nonstructural protein PB1-F2 also contributes to virulence through four mechanisms: inducing apoptosis, IFN suppression, increasing viral replication rates or delaying viral clearance, and increasing inflammation. […] NS1, another nonstructural protein, interferes with antiviral response and exhibits both proapoptotic and antiapoptotic activities.
  • #2 Influenza A H1N1 | Symptoms, Treatment & Prevention | Britannica
    https://www.britannica.com/science/influenza-A-H1N1
    influenza A H1N1, virus that is best known for causing widespread outbreaks, including epidemics and pandemics, of acute upper or lower respiratory tract infection. […] Influenza A H1N1 is subject to antigenic driftconstant, rapid viral evolution driven by mutations in the genes that encode the H and N antigen proteins. […] Viral evolution is facilitated by animals such as pigs and birds, which serve as reservoirs of various subtypes and strains of influenza A viruses. […] Reassortment represents another process by which new strains of influenza A H1N1 can be generated. […] Strains of the H1N1 influenza subtype circulate constantly in human populations worldwide and thus are continually evolving and evading the human immune system. […] The influenza pandemic of 191819, the most destructive influenza outbreak in history and one of the most severe disease pandemics ever encountered, was caused by an H1N1 virus.
  • #2 Swine Influenza(a H1n1) | Official Website of Department of Health & Family Welfare, Government of Puducherry, India.
    https://health.py.gov.in/swine-influenzaa-h1n1
    Flu viruses are spread mainly from person to person through coughing or sneezing of people with influenza. […] Infected people may be able to infect others beginning 1 day before symptoms develop and up to 7 or more days after becoming sick. […] People with swine influenza virus infection should be considered potentially contagious as long as they are symptomatic and possible for up to 7 days following illness onset. […] There is no vaccine available right now to protect against swine flu. […] Swine influenza viruses are not spread by food. You cannot get swine influenza from eating pork or pork products. Eating properly handled and cooked pork products is safe.
  • #2 Swine Flu: Risk Factors, Causes & Symptoms
    https://www.healthline.com/health/swine-flu
    Swine flu, also known as the H1N1 virus, is a relatively new strain of an influenza virus that causes symptoms similar to the regular flu. It originated in pigs but is spread primarily from person to person. […] Swine flu is caused by a strain of influenza virus that usually only infects pigs. Unlike typhus, which can be transmitted by lice or ticks, transmission usually occurs from person to person, not animal to person. […] Swine flu is very contagious. The disease is spread through saliva and mucus particles. People may spread it by: sneezing, coughing, touching a germ-covered surface and then touching their eyes or nose. […] Most cases of swine flu don’t require medication for treatment. You don’t need to see a doctor unless you’re at risk for developing medical complications from the flu. You should focus on relieving your symptoms and preventing the spread of the H1N1 to other people. […] Severe cases of swine flu can be fatal. Most fatal cases occur in those with underlying chronic medical conditions, such as HIV or AIDS. The majority of people with swine flu recover and can anticipate a normal life expectancy.
  • #2 Investigation of Pathogenesis of H1N1 Influenza Virus and Swine Streptococcus suis Serotype 2 Co-Infection in Pigs by Microarray Analysis | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124086
    The increased virulence of co-infection might also be attributed to the enhanced viral replication or SS2 growth. […] The H1N1-SS2 co-infection is proposed to induce stronger inflammatory responses, which caused more severe inflammatory damage in the lungs. […] The microarray analysis results also indicated that more genes involved in apoptosis pathway were regulated. In the H1N1-SS2 group, members of the TNFR superfamily (TNFRSF10A, TNFRSF1B, and TNFRSF8), caspase family (CASP2, CASP3, and CASP4), BCL2-like genes (BCL2L11 and BCL2L14), FASLG, and GZME were upregulated. […] The impacts of apoptosis on the viral replication vary depending on different virus. Infected cells possibly release the infectious viral particles into micro-environment, which then infect the nearby cells and trigger apoptosis. […] Therefore, co-infection by H1N1 and SS2 could potentiate virulence by causing severe apoptosis.
  • #2 Pathogenesis and transmission of swine-origin 2009 A(H1N1) influenza virus in ferrets
    https://repub.eur.nl/pub/25229
    The swine-origin A(H1N1) influenza virus that has emerged in humans in early 2009 has raised concerns about pandemic developments. In a ferret pathogenesis and transmission model, the 2009 A(H1N1) influenza virus was found to be more pathogenic than a seasonal A(H1N1) virus, with more extensive virus replication occurring in the respiratory tract. […] Replication of seasonal A(H1N1) virus was confined to the nasal cavity of ferrets, but the 2009 A(H1N1) influenza virus also replicated in the trachea, bronchi, and bronchioles. Virus shedding was more abundant from the upper respiratory tract for 2009 A(H1N1) influenza virus as compared with seasonal virus, and transmission via aerosol or respiratory droplets was equally efficient. […] These data suggest that the 2009 A(H1N1) influenza virus has the ability to persist in the human population, potentially with more severe clinical consequences.
  • #2 Transmission and Pathogenesis of Swine-Origin 2009 A(H1N1) Influenza Viruses in Ferrets and Mice
    https://dspace.mit.edu/handle/1721.1/88974
    Recent reports of mild to severe influenza-like illness in humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better understand the pathogenesis and transmission of these viruses in mammals. […] In this study, selected 2009 A(H1N1) influenza isolates were assessed for their ability to cause disease in mice and ferrets and compared with a contemporary seasonal H1N1 virus for their ability to transmit to nave ferrets through respiratory droplets. […] In contrast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, replicated to higher titers in lung tissue, and were recovered from the intestinal tract of intranasally inoculated ferrets. […] The 2009 A(H1N1) influenza viruses exhibited less efficient respiratory droplet transmission in ferrets in comparison with the highly transmissible phenotype of a seasonal H1N1 virus. […] Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by characterizing the binding specificity of the viral hemagglutinin to the sialylated glycan receptors (in the human host) by use of dose-dependent direct receptor-binding and human lung tissue-binding assays.
  • #2 H1N1 Influenza (Swine Flu): Practice Essentials, Background, Epidemiology
    https://emedicine.medscape.com/article/1807048-overview
    The ability to trace outbreaks of swine flu in humans dates back to investigation of the 1918 Spanish influenza pandemic, which infected one third of the worlds population (an estimated 500 million people) and caused approximately 50 million deaths. […] In humans, the severity of swine influenza can vary from mild to severe. […] Treatment largely is supportive and consists of bedrest, increased fluid consumption, cough suppressants, and antipyretics and analgesics (eg, acetaminophen, nonsteroidal anti-inflammatory drugs) for fever and myalgias. Severe cases may require intravenous hydration and other supportive measures. Antiviral agents may also be considered for treatment or prophylaxis. […] A review of medical records from the 2009 US pandemic found hospitalized patients with pandemic H1N1 and pneumonia were at risk for severe outcomes including ARDS, sepsis, and death. However, patients often received delayed antiviral treatment (2 days after illness onset). Patients with H1N1 and pneumonia should receive early and aggressive treatment with antibiotics and influenza antiviral agents. […] In a multicenter study in Britain consisting of over 1500 patients, independent predictors of severe outcome included age 55 to 64 years, certain chronic lung diseases, underlying neurological disease, obesity, delayed admission (5 days after illness onset), pneumonia, and others.
  • #2 Swine Flu (H1N1): What Is It, Causes, Treatments & Prevention
    https://my.clevelandclinic.org/health/diseases/23928-swine-flu-h1n1
    If youre very ill, your healthcare provider may prescribe an antiviral medicine. Antiviral drugs such as oseltamivir (Tamiflu) or zanamivir (Relenza) can kill the virus. These drugs can shorten the time youre sick and help ease your symptoms. Antiviral drugs work best if you start taking them when your symptoms begin. […] Swine flu (H1N1) once caused a serious worldwide pandemic. The virus is under control today, but people can and do still get very sick from H1N1. If you do get sick, make sure to get plenty of rest, drink fluids and call your healthcare provider if symptoms worsen.
  • #2 Effect of Prior Influenza A(H1N1)pdm09 Virus Infection on Pathogenesis and Transmission of Human Influenza A(H5N1) Clade 2.3.4.4b Virus in Ferret Model – Volume 31, Number 3—March 2025 – Emerging Infectious Diseases journal – CDC
    https://wwwnc.cdc.gov/eid/article/31/3/24-1489_article
    Moreover, direct-contact transmission was abolished when either the donor or recipient animals had prior H1N1 immunity. […] Our results showed that prior pH1N1 virus infection more effectively reduced the replication and transmission of H5N1 virus than it did H7N9 virus in a ferret model. […] Those results suggest that pH1N1 virus immunity may confer some level of protection against H5N1 clade 2.3.4.4.b virus in humans.
  • #2 Researchers Discover the 2009 Swine Flu Pandemic Originated in Mexico | Mount Sinai – New York
    https://www.mountsinai.org/about/newsroom/2016/researchers-discover-the-2009-swine-flu-pandemic-originated-in-mexico
    Determining the original location of the 2009 swine flu, known as an A/H1N1 pathogen, lends a note of caution to evolving efforts to track problematic animal and bird viruses, Dr. Garcia-Sastre says. […] Flu viruses have eight mini chromosomes and when two different strains infect the same cell they can exchange genetic segments — a process called reassortment. […] The 2009 A/H1N1 was also a derivative of two different strains of swine influenza — one that had been circulating in Europe and Asia and another that was circulating in the Americas, especially North America. […] The 2009 swine virus was therefore a “quadruple” reassortment, Dr. Garcia-Sastre says. […] By solving the origins and the reassortments that led to the 2009 A/H1N1 pandemic, researchers might be able to study existing “brothers and sisters” of the virus to understand the type of mutations needed to allow a virus to jump into humans. […] Worldwide surveillance of active flu in pigs is crucial because swine are a common global commodity, Dr. Garcia-Sastre says.
  • #2 Swine flu lineage has passed from humans to pigs 400 times
    https://sciencemediacentre.es/en/reactions-lineage-so-called-swine-flu-has-passed-humans-pigs-almost-400-times-2009
    It is well known that the pig is a key species in the emergence of zoonotic influenza viruses. In fact, it is considered the main shaker species, since it is susceptible to swine, human and bird flu viruses. […] Since the start of the H1N1 influenza A (pdm2009) pandemic, numerous cases of transmission of this pandemic virus from humans to pigs (reverse zoonosis) have been documented in Europe and the USA. […] The introduction and establishment of new viruses of human origin in pigs increases the heterogeneity of the viruses in this species and increases the chances of the origin of swine flu strains capable of inverse transmission to humans and causing new pandemics. […] This evolutionary closeness between swine and human influenza viruses explains the relative ease of reciprocal transmission of viruses between the two species. For this reason, close and constant surveillance of influenza viruses in both species is absolutely necessary to anticipate possible emergencies of swine flu viruses with pandemic potential and the reissue of another pandemic similar to or with worse consequences than the one suffered in 2009.