Materiały źródłowe

• #1 Rubella – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559040/

  Rubella, or German measles, is a mild viral infection that typically occurs in children and non-immune young adults. It typically begins with low-grade fever, malaise, and lymphadenopathy, followed by a brief generalized erythematous maculopapular rash. […] In nonpregnant individuals, rubella is generally a self-limited and benign infection. However, maternal rubella infection, especially during the first 10 weeks of gestation, can result in miscarriage, fetal death, or severe birth defects collectively known as congenital rubella syndrome (CRS). […] Rubella virus is the sole member of the genus Rubivirus within the newly classified Matonaviridae family. It is a single-stranded, positive sense enveloped RNA virus. Rubella virus encodes two non-structural proteins (p90 and p150) and three structural proteins; glycoprotein (E1 and E2) and the capsid protein (CP). The E1 protein is responsible for receptor-mediated endocytosis and induces the immune response through hemagglutination-neutralizing epitopes.

• #1 Pediatric Rubella: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968523-overview

  The usual portal of entry of rubella virus is the respiratory epithelium of the nasopharynx. The virus is transmitted via the aerosolized particles from the respiratory tract secretions of infected individuals. The virus attaches to and invades the respiratory epithelium. It then spreads hematogenously (primary viremia) to regional and distant lymphatics and replicates in the reticuloendothelial system. This is followed by a secondary viremia that occurs 6-20 days after infection. During this viremic phase, rubella virus can be recovered from different body sites including lymph nodes, urine, cerebrospinal fluid (CSF), conjunctival sac, breast milk, synovial fluid, and lungs. Viremia peaks just before the onset of rash and disappears shortly thereafter. An infected person begins to shed the virus from the nasopharynx 3-8 days after exposure for 6-14 days after onset of the rash.

• #1 Rubella (German measles) revisited | HKMJ

  https://www.hkmj.org/abstracts/v25n2/134.htm

  Postnatally acquired rubella is transmitted mainly via inhalation of aerosolised particles from the respiratory tract secretions of an infected individual. The virus infects cells in the upper respiratory tract of the susceptible host through receptor-mediated endocytosis. Initial replication occurs in the nasopharyngeal cells and lymphoid tissue of the nasopharynx and upper respiratory tract. […] Viraemia occurs 5 to 7 days after inoculation, disseminating the virus to multiple organs including the skin, lymph nodes, and, in a gravid patient, the placenta. The maculopapular rash occurs 2 to 8 days after the onset of viraemia and resolves as the humoral immune response develops and at this stage, the viraemia is terminated. […] In a susceptible gravid patient, after infecting the placenta, the virus may cross the placenta, and spread through the vascular system of the developing fetus. Fetal damage may result from necrosis in the epithelium of chorionic villi, direct viral damage of infected cells by apoptosis, viral inhibition of mitosis and restricted development of precursor cells, and cytopathic damage to endothelial cells of blood vessels with resultant ischaemia in developing organs.

• #1 Rubella – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559040/

  Humans are the only known reservoir for rubella. The virus is contracted through person-to-person contact via aerosolized particles from the respiratory tract secretions of affected individuals. After infecting the cells of the susceptible host through receptor-mediated endocytosis, the virus replicates in the nasopharyngeal cells and then spreads to the regional lymphoid tissue of the nasopharynx and upper respiratory tract. This process is followed by a viremic phase, which is characterized by hematogenous dissemination of the virus to multiple organs, and it usually occurs 5 to 7 days after inoculation. […] In congenital rubella syndrome (CRS), fetal infection occurs transplacentally during the maternal viremic phase. The risk of transmission to the fetus depends on the time of maternal infection; when infection with rubella occurs before 10 weeks of gestation, it may cause multiple fetal defects in up to 90% of cases. The risk of congenital defects declines with infection later in gestation. The pathogenesis of CRS is multifactorial and not well understood. In CRS, damage to the fetus may result from several mechanisms including epithelial necrosis of chorionic villi, apoptosis of infected cells by direct viral damage, inhibition of mitosis, and restricted development of precursor cells by the virus, and cytopathic damage to endothelial cells of blood vessels resulting in ischemia of developing organs.

• #1 Rubella (German measles) revisited | HKMJ

  https://www.hkmj.org/abstracts/v25n2/134.htm

  Maternal rubella infection during pregnancy does not always result in vertical transmission of the virus to the fetus. The risk of fetal infection varies depending upon the time of maternal infection. Fetal infection rates are approximately 80% in the first trimester, 25% in the late second trimester, 35% at 27 to 30 weeks gestation, and close to 100% beyond 36 weeks gestation. […] The estimated risk for fetal malformation is approximately 90%, 33%, 11%, 24% and 0% when maternal infection occurs before 11 weeks, at 11 to 12 weeks, at 13 to 14 weeks, at 15 to 16 weeks, and after 20 weeks of gestation, respectively. This can be explained by passive transfer of maternal antibodies and by development of fetal humoral and cell-mediated immune responses with time.

• #1 Pediatric Rubella: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968523-overview

  Fetal infection occurs transplacentally during the maternal viremic phase, but the mechanisms by which rubella virus causes fetal damage are poorly understood. The fetal defects observed in congenital rubella syndrome are likely secondary to vasculitis resulting in tissue necrosis without inflammation. Another possible mechanism is direct viral damage of infected cells. Studies have demonstrated that cells infected with rubella in the early fetal period have reduced mitotic activity. This may be the result of chromosomal breakage or due to production of a protein that inhibits mitosis. Regardless of the mechanism, any injury affecting the fetus in the first trimester (during the phase of organogenesis) results in congenital organ defects.

• #1 Molecular aspects of the teratogenesis of rubella virus | Biological Research | Full Text

  https://biolres.biomedcentral.com/articles/10.1186/s40659-019-0254-3

  The most serious effect of RV infection is its teratogenicity. The birth defects seen in infants include blindness, deafness, congenital heart disease, mental retardation and neurological complications, all of them collectively referred to as congenital rubella syndrome (CRS). […] The teratogenic effect of rubella appears to be direct as well as indirect. Restricted damage to certain organs reflects a varied response of the fetal cells to virus infection. For example, rubella induced apoptosis is seen only in non proliferative and differentiated cells, while apoptosis was not induced in proliferative cells, which would promote viral persistence. The indirect effect of rubella infection includes secretion of interferon and other cytokines by the infected cells that in turn can disrupt growth and proliferation pathways in developing and differentiating cells leading to congenital effects. This is supported by the reports of upregulation of interferons and cytokines in rubella infected human embryo fibroblast.

• #1 Molecular aspects of the teratogenesis of rubella virus | Biological Research | Full Text

  https://biolres.biomedcentral.com/articles/10.1186/s40659-019-0254-3

  In conclusion, RV has a small genome and codes for only five proteins. Based on reports through studies on molecular and cell biology, it is evident that several proteins of the host interact with many of these viral proteins to bring about the teratogenic effects. It is interesting to note that some of the host proteins that regulate cell division and cell growth have been found to associate with RV p90. Furthermore replication of the virus in the host cell, directly and indirectly affects the expression of genes involved in the development of sensory organs. Also, there is evidence of cytoskeleton and mitochondrial changes during RV infection. Thus, the lifelong effects that RV inflicts on the developing fetus are cumulative with the outcome arising from the host RV protein interaction.

• #1 Rubella Virus | Concise Medical Knowledge

  https://www.lecturio.com/concepts/rubella-virus/

  Prenatal: […] Direct viremia via placental transmission. […] Outcome depends on gestational age and is likely due to immature fetal host defenses. […] Risk of infection and associated congenital defects decreases with gestational age: 40%-60% chance if the mother is infected during the 1st 2 months of gestation, 30%-35% chance during the 3rd month of gestation, 10% chance during the 4th month of gestation. […] Virions may affect virtually any fetal organ system. […] Postnatal primary infections with rubella undergo a sequential pathogenic process: Inoculation through the respiratory tract, Attachment to respiratory tract cell membranes (entry of the virion into the host cell occurs via transportation into endosomes), Multiplication in host cell cytoplasm over 2-3 weeks, Exocytosis via an unclear mechanism, Infiltration of local lymph nodes causing constitutional symptoms and lymphadenopathy, Development of viremia (virus is detected in the blood and respiratory secretions), Multiplication in the cells of other organs, Development of fever and rash detected in the blood. […] Before rash resolution, disappearance of detectable virus in the blood as the antibodies surge. […] IgG antibodies confer future immunity, but reinfection can occur.

• #1 Togaviruses: Rubella Virus – Medical Microbiology – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK8200/

  Rubella virus multiplies in cells of the respiratory system; this is followed by viremic spread to target organs. Congenital infection is transmitted transplacentally. […] The virus almost certainly multiplies in cells of the respiratory tract, extends to local lymph nodes, and then undergoes viremic spread to target organs. Subsequent additional replication in selected target organs, such as the spleen and lymph nodes, leads to a secondary viremia with wide distribution of rubella virus. […] Rubella infection in the first 3 or 4 months of pregnancy provides opportunities during the period of maternal viremia for invasion of the placenta and subsequent fetal infection. Development of infection probably depends upon gestational age. […] During fetal infection, the virus can multiply in and damage virtually any organ system. Pathogenesis of the congenital defects is not fully understood; however, a number of mechanisms have been proposed. Cell culture studies show that the virus produces chromosomal abnormalities, slows cellular growth rates, and causes cell lysis and death in some cell types; these effects appear capable of producing the characteristic abnormalities of cell structure and function. In addition, rubella infection induces angiopathy of early placental and embryonic tissues, causing interference with the fetal blood supply and subsequent compromised growth and/or malformation of the fetus. In the congenitally infected fetus and infant, virus persistence occurs in the presence of neutralizing antibodies; immunological tolerance does not develop.

• #1 Rubella – Wikipedia

  https://en.wikipedia.org/wiki/Rubella

  Rubella is caused by the rubella virus, in the genus Rubivirus from the family Matonaviridae, that is enveloped and has a single-stranded RNA genome. The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. The virus has teratogenic properties and is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them. […] Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are involved in virus infection or non-resolution of the disease.

• #1 Lupus may compromise long-term rubella immunity in adolescents | Lupus Foundation of America

  https://www.lupus.org/news/lupus-may-compromise-longterm-rubella-immunity-in-adolescents

  Rubella, also known as German measles, is a contagious infection caused by the rubella virus. […] Possible causes for the reduction in protective antibodies against rubella may be attributed to the disease mechanism, lupus activity, or medications used to manage lupus. […] Ultimately, more research investigating how autoimmune diseases, specifically lupus, impact long-term immunity conferred by vaccination is needed.

• #1 Rubella and Congenital Rubella (German Measles) – Journal of Long-Term Effects of Medical Implants, Volume 15, 2005, Issue 3 – Begell House Digital Library

  https://www.dl.begellhouse.com/journals/1bef42082d7a0fdf,69622d0e4ea6cf4b,4fb4b32d494cf55c.html

  Rubella, also known as German measles, is usually a very mild infection that can have devastating effects in certain instances. It is a pleomorphic RNA virus in the Togaviridae family of the genus Rubivirus. […] Infection during the first 12 weeks of pregnancy results in congenital infection and/or miscarriage in 80-90% of cases. The congenital rubella syndrome (CRS) involves multiple organ systems and has a long period of active infection and virus shedding in the postnatal period. […] Virus is present in nasopharyngeal secretions, blood, feces, and urine during the clinical illness, although patients with subclinical disease are also infectious. The virus is spread via oral droplets and is shed in the nasopharynx for approximately 7 days before and after the rash is visible. […] CRS includes a configuration of anomalies, including nerve deafness, cataracts, cardiac anomalies (usually pulmonary artery and valvular stenosis, and patent ductus arteriosis), and mental retardation, with late complications including diabetes, thyroid disease, growth hormone deficiency, and progressive panencephalitis.

• #1 4 Measles, Mumps, and Rubella Vaccine | Adverse Effects of Vaccines: Evidence and Causality | The National Academies Press

  https://nap.nationalacademies.org/read/13164/chapter/6

  Rubella virus infection during pregnancy can lead to congenital rubella infection in neonates. The disease outcome is directly correlated to the age of the fetus at the time of infection, with younger fetuses experiencing more severe disease. Infections within the first 2 months of pregnancy can cause multiple congenital defects or spontaneous abortion in 65 to 85 percent of women. Infections in the third month and fourth month are associated with a single defect in 30 to 35 percent and 10 percent of cases, respectively. Commonly associated defects include transient thrombocytopenia purpura and meningoencephalitis, as well as permanent and developmental manifestations such as hearing loss, pulmonic stenosis, mental retardation, and behavioral disorders. Other less common manifestations include myocardial abnormalities, hepatitis, and seizure disorders. Studies have also shown that diabetes mellitus occurs 50 times more frequently in children with congenital rubella, and insulin-dependent diabetes has been reported in 40 percent of adults who were congenitally infected with rubella during the 1942 rubella epidemic.

• #2 Rubella | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/28669

  Rubella virus is the sole member of the genus Rubivirus within the newly classified Matonaviridae family. It is a single-stranded, positive sense enveloped RNA virus. Rubella virus encodes two non-structural proteins (p90 and p150) and three structural proteins; glycoprotein (E1 and E2) and the capsid protein (CP). The E1 protein is responsible for receptor-mediated endocytosis and induces the immune response through hemagglutination-neutralizing epitopes. The virus is sensitive to heat (temperature 56C), ultraviolet light, and extremes of pH (pH 6.8 or 8.1). […] Humans are the only known reservoir for rubella. The virus is contracted through person-to-person contact via aerosolized particles from the respiratory tract secretions of affected individuals. After infecting the cells of the susceptible host through receptor-mediated endocytosis, the virus replicates in the nasopharyngeal cells and then spreads to the regional lymphoid tissue of the nasopharynx and upper respiratory tract. This process is followed by a viremic phase, which is characterized by hematogenous dissemination of the virus to multiple organs, and it usually occurs 5 to 7 days after inoculation. The exanthem appears approximately 2 to 8 days after the onset of viremia and resolves 3 days later as the humoral immune response develops. An infected individual is contagious from 8 days before to 8 days after the onset of the rash. Immunity acquired after recovering from natural infection or through vaccination is life-long; however, reinfection has been reported after both wild type rubella infection and after receiving one dose of rubella vaccine.

• #2 Rubella – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK559040/

  Humans are the only known reservoir for rubella. The virus is contracted through person-to-person contact via aerosolized particles from the respiratory tract secretions of affected individuals. After infecting the cells of the susceptible host through receptor-mediated endocytosis, the virus replicates in the nasopharyngeal cells and then spreads to the regional lymphoid tissue of the nasopharynx and upper respiratory tract. This process is followed by a viremic phase, which is characterized by hematogenous dissemination of the virus to multiple organs, and it usually occurs 5 to 7 days after inoculation. […] In congenital rubella syndrome (CRS), fetal infection occurs transplacentally during the maternal viremic phase. The risk of transmission to the fetus depends on the time of maternal infection; when infection with rubella occurs before 10 weeks of gestation, it may cause multiple fetal defects in up to 90% of cases. The risk of congenital defects declines with infection later in gestation. The pathogenesis of CRS is multifactorial and not well understood. In CRS, damage to the fetus may result from several mechanisms including epithelial necrosis of chorionic villi, apoptosis of infected cells by direct viral damage, inhibition of mitosis, and restricted development of precursor cells by the virus, and cytopathic damage to endothelial cells of blood vessels resulting in ischemia of developing organs.

• #2 Rubella pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Rubella_pathophysiology

  The pathophysiology of rubella is not completely understood. Viral replication in the respiratory epithelium occurs following transmission of the virus via contact with droplet secretions from an infected person. Viremia subsequently ensues, with the onset of the rubella rash occurring at the peak of viremia. […] The pathophysiology of rubella infection involves the following processes: […] The transmission of infection is via person-person spread through droplets that are shed from respiratory secretions of infected persons. […] Viral replication occurs in the respiratory epithelium, with subsequent spread of the virus to the regional lymph nodes. […] Viremia ensues and subsequent seeding of viremia to multiple organs may occur (including the placenta in pregnant women, which results in congenital rubella syndrome).

• #2 Rubella pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Rubella_pathophysiology

  The onset of viremia is usually between 8-9 days after exposure, peaking at 10-17 days. […] The onset of rash often occurs 16-18 days after exposure (around the peak of viremia). […] Approximately 10 days after infection, viral shedding from the nasopharynx begins. […] Viral shedding may continue 1 week before the rash appears to about 5-14 days after the disappearance of the rash. […] The infected patient is contagious 5 days before the onset of the rash to 6 days after the appearance of the rash.

• #2

  https://www.microbiologybook.org/mhunt/rubella.htm

  Rubella virus is the only member of the Rubrivirus genus of the Togavirus family. […] Rubella virus (figure 1) is the only member of the Rubivirus genus of the Togavirus family. Unlike most Togaviruses it is NOT arthropod-borne, but is acquired via the respiratory route. It is an enveloped (toga=cloak), non-segmented, positive sense, RNA virus and replicates in the cytoplasm. Its nucleocapsid has icosahedral symmetry (figure 2). There is only one major antigenic type. […] The initial site of infection is the upper respiratory tract. The virus replicates locally (in the epithelium, lymph nodes) leading to viremia and spread to other tissues. As a result the disease symptoms develop. Rash, if it occurs, (table 1) starts after an incubation period of approximately 2 weeks (12 to 23 days) from the initial infection. There is probably an immunological basis for the rash (since it occurs as antibody titers rise).

• #2 Chapter 20: Rubella | Pink Book | CDC

  https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-20-rubella.html

  Following respiratory transmission, the virus replicates in the nasopharynx and regional lymph nodes. […] In a pregnant woman, placental infection occurs during viremia and may lead to transplacental fetal infection. Fetal damage occurs through destruction of cells, as well as disruption of cell division. Fetal infection often results in a persistent infection typically leading to hearing impairment and ocular and cardiovascular abnormalities.

• #2 4 Measles, Mumps, and Rubella Vaccine | Adverse Effects of Vaccines: Evidence and Causality | The National Academies Press

  https://nap.nationalacademies.org/read/13164/chapter/6

  Rubella virus infection during pregnancy can lead to congenital rubella infection in neonates. The disease outcome is directly correlated to the age of the fetus at the time of infection, with younger fetuses experiencing more severe disease. Infections within the first 2 months of pregnancy can cause multiple congenital defects or spontaneous abortion in 65 to 85 percent of women. Infections in the third month and fourth month are associated with a single defect in 30 to 35 percent and 10 percent of cases, respectively. Commonly associated defects include transient thrombocytopenia purpura and meningoencephalitis, as well as permanent and developmental manifestations such as hearing loss, pulmonic stenosis, mental retardation, and behavioral disorders. Other less common manifestations include myocardial abnormalities, hepatitis, and seizure disorders. Studies have also shown that diabetes mellitus occurs 50 times more frequently in children with congenital rubella, and insulin-dependent diabetes has been reported in 40 percent of adults who were congenitally infected with rubella during the 1942 rubella epidemic.

• #2 Rubella | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/28669

  In congenital rubella syndrome (CRS), fetal infection occurs transplacentally during the maternal viremic phase. The risk of transmission to the fetus depends on the time of maternal infection; when infection with rubella occurs before 10 weeks of gestation, it may cause multiple fetal defects in up to 90% of cases. The risk of congenital defects declines with infection later in gestation. The pathogenesis of CRS is multifactorial and not well understood. In CRS, damage to the fetus may result from several mechanisms including epithelial necrosis of chorionic villi, apoptosis of infected cells by direct viral damage, inhibition of mitosis, and restricted development of precursor cells by the virus, and cytopathic damage to endothelial cells of blood vessels resulting in ischemia of developing organs.

• #2 Molecular aspects of the teratogenesis of rubella virus | Biological Research | Full Text

  https://biolres.biomedcentral.com/articles/10.1186/s40659-019-0254-3

  The most serious effect of RV infection is its teratogenicity. The birth defects seen in infants include blindness, deafness, congenital heart disease, mental retardation and neurological complications, all of them collectively referred to as congenital rubella syndrome (CRS). […] The teratogenic effect of rubella appears to be direct as well as indirect. Restricted damage to certain organs reflects a varied response of the fetal cells to virus infection. For example, rubella induced apoptosis is seen only in non proliferative and differentiated cells, while apoptosis was not induced in proliferative cells, which would promote viral persistence. The indirect effect of rubella infection includes secretion of interferon and other cytokines by the infected cells that in turn can disrupt growth and proliferation pathways in developing and differentiating cells leading to congenital effects. This is supported by the reports of upregulation of interferons and cytokines in rubella infected human embryo fibroblast.

• #2

  https://www.microbiologybook.org/mhunt/rubella.htm

  The risk to a fetus is highest in the first few weeks of pregnancy and then declines in terms of both frequency and severity, although there is still some risk in the second trimester. The virus infects the placenta and then spreads to the fetus. […] Virus from congenital infections persists after birth. Those with congenital infections can infect others after birth for a year or more. Virus occurs in naso-pharyngeal secretions, urine and feces. Later on, patients with congenital rubella syndrome may develop additional complications including diabetes mellitus (up to 20%), thyroid dysfunction, growth hormone deficiency, ocular complications.

• #2 4 Measles, Mumps, and Rubella Vaccine | Adverse Effects of Vaccines: Evidence and Causality | The National Academies Press

  https://nap.nationalacademies.org/read/13164/chapter/6

  Rubella, also known as German measles, is caused by an enveloped, positive-sense RNA togavirus of the genus Rubivirus. The rubella virus genome consists of approximately 9,800 nucleotides, and the virus can be divided into two clades and at least seven genotypes. Maturing by budding from the cell membrane, rubella virus is relatively unstable and vulnerable to chemical inactivation, extremes of pH and heat, lipid solvents, and ultraviolet light. […] Rubella is spread through contact with infectious respiratory secretions, and replication occurs in the nasopharynx of the infected individual. Rubella infections are subclinical in 25 to 50 percent of cases. In those cases in which clinical illness develops, the beginning of the 12- to 23-day incubation period is largely asymptomatic. By the end of the second week, virus can be isolated from the blood and symptoms of conjunctivitis, low-grade fever, lymphadenopathy, and malaise are present. A rash follows, spreading downwards from the face before fading within 1 to 3 days. Rubella illness in a child or adult is usually benign, although arthritis and arthralgia have been observed in association with viral replication in the synovial cavity of the joints. Other complications of rubella include encephalitis, Guillain-Barr syndrome, progressive rubella panencephalitis, and thrombocytopenia.

• #2 Rubella (German Measles or Three-Day Measles)

  https://www.health.ny.gov/diseases/communicable/rubella/fact_sheet.htm

  Rubella is a highly contagious viral disease characterized by slight fever, mild rash and swollen glands. […] Although most cases are mild, if rubella is contracted early in pregnancy, it can spread from the mother to her developing baby through the bloodstream and result in birth defects and/or fetal death. […] Up to 85 percent of infants infected with rubella in the first trimester of pregnancy will suffer birth defects and/or neurologic abnormalities (Congenital Rubella Syndrome, CRS). […] Rubella infection is dangerous because of its ability to damage an unborn baby. […] The danger would be to pregnant women who, if infected, could pass the disease to their infants (fetuses) causing CRS. […] Congenital rubella syndrome occurs among at least 25 percent of infants born to women who had rubella during the first three months of pregnancy. Infection of a pregnant woman can result in a miscarriage, stillbirth or the birth of an infant with abnormalities which may include deafness, blindness, cataracts, heart defects, mental retardation, liver and spleen damage.

• #3 4 Measles, Mumps, and Rubella Vaccine | Adverse Effects of Vaccines: Evidence and Causality | The National Academies Press

  https://nap.nationalacademies.org/read/13164/chapter/6

  Rubella, also known as German measles, is caused by an enveloped, positive-sense RNA togavirus of the genus Rubivirus. The rubella virus genome consists of approximately 9,800 nucleotides, and the virus can be divided into two clades and at least seven genotypes. Maturing by budding from the cell membrane, rubella virus is relatively unstable and vulnerable to chemical inactivation, extremes of pH and heat, lipid solvents, and ultraviolet light. […] Rubella is spread through contact with infectious respiratory secretions, and replication occurs in the nasopharynx of the infected individual. Rubella infections are subclinical in 25 to 50 percent of cases. In those cases in which clinical illness develops, the beginning of the 12- to 23-day incubation period is largely asymptomatic. By the end of the second week, virus can be isolated from the blood and symptoms of conjunctivitis, low-grade fever, lymphadenopathy, and malaise are present. A rash follows, spreading downwards from the face before fading within 1 to 3 days. Rubella illness in a child or adult is usually benign, although arthritis and arthralgia have been observed in association with viral replication in the synovial cavity of the joints. Other complications of rubella include encephalitis, Guillain-Barr syndrome, progressive rubella panencephalitis, and thrombocytopenia.

• #3 Does rubella virus have an animal origin? | Friedrich-Loeffler-Institut

  https://www.fli.de/en/press/press-releases/press-singleview/does-rubella-virus-have-an-animal-origin/

  Isle of Riems, 7 October 2020. Up to now, humans were considered the only natural host of rubella virus, the causative agent of rubella (German measles). However, the origin of rubella virus was still unknown. […] Both viruses show strong structural similarities to rubella virus and indicate that it originates from animals. […] The comprehensive analysis of the two novel viruses, but also the search for possible further animal reservoirs and other rubella virus-like pathogens are now an important field of research to better understand the origin of human rubella viruses, says Prof. Dr. Martin Beer, study leader at FLI. […] Knowledge about the origin of the virus can make an important contribution to achieving this goal.

• #3 Rubella (German measles) revisited | HKMJ

  https://www.hkmj.org/abstracts/v25n2/134.htm

  Postnatally acquired rubella is transmitted mainly via inhalation of aerosolised particles from the respiratory tract secretions of an infected individual. The virus infects cells in the upper respiratory tract of the susceptible host through receptor-mediated endocytosis. Initial replication occurs in the nasopharyngeal cells and lymphoid tissue of the nasopharynx and upper respiratory tract. […] Viraemia occurs 5 to 7 days after inoculation, disseminating the virus to multiple organs including the skin, lymph nodes, and, in a gravid patient, the placenta. The maculopapular rash occurs 2 to 8 days after the onset of viraemia and resolves as the humoral immune response develops and at this stage, the viraemia is terminated. […] In a susceptible gravid patient, after infecting the placenta, the virus may cross the placenta, and spread through the vascular system of the developing fetus. Fetal damage may result from necrosis in the epithelium of chorionic villi, direct viral damage of infected cells by apoptosis, viral inhibition of mitosis and restricted development of precursor cells, and cytopathic damage to endothelial cells of blood vessels with resultant ischaemia in developing organs.

• #3 Rubella | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/28669

  Rubella virus is the sole member of the genus Rubivirus within the newly classified Matonaviridae family. It is a single-stranded, positive sense enveloped RNA virus. Rubella virus encodes two non-structural proteins (p90 and p150) and three structural proteins; glycoprotein (E1 and E2) and the capsid protein (CP). The E1 protein is responsible for receptor-mediated endocytosis and induces the immune response through hemagglutination-neutralizing epitopes. The virus is sensitive to heat (temperature 56C), ultraviolet light, and extremes of pH (pH 6.8 or 8.1). […] Humans are the only known reservoir for rubella. The virus is contracted through person-to-person contact via aerosolized particles from the respiratory tract secretions of affected individuals. After infecting the cells of the susceptible host through receptor-mediated endocytosis, the virus replicates in the nasopharyngeal cells and then spreads to the regional lymphoid tissue of the nasopharynx and upper respiratory tract. This process is followed by a viremic phase, which is characterized by hematogenous dissemination of the virus to multiple organs, and it usually occurs 5 to 7 days after inoculation. The exanthem appears approximately 2 to 8 days after the onset of viremia and resolves 3 days later as the humoral immune response develops. An infected individual is contagious from 8 days before to 8 days after the onset of the rash. Immunity acquired after recovering from natural infection or through vaccination is life-long; however, reinfection has been reported after both wild type rubella infection and after receiving one dose of rubella vaccine.

• #3 Rubella pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Rubella_pathophysiology

  The onset of viremia is usually between 8-9 days after exposure, peaking at 10-17 days. […] The onset of rash often occurs 16-18 days after exposure (around the peak of viremia). […] Approximately 10 days after infection, viral shedding from the nasopharynx begins. […] Viral shedding may continue 1 week before the rash appears to about 5-14 days after the disappearance of the rash. […] The infected patient is contagious 5 days before the onset of the rash to 6 days after the appearance of the rash.

• #3 Rubella | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/28669

  In congenital rubella syndrome (CRS), fetal infection occurs transplacentally during the maternal viremic phase. The risk of transmission to the fetus depends on the time of maternal infection; when infection with rubella occurs before 10 weeks of gestation, it may cause multiple fetal defects in up to 90% of cases. The risk of congenital defects declines with infection later in gestation. The pathogenesis of CRS is multifactorial and not well understood. In CRS, damage to the fetus may result from several mechanisms including epithelial necrosis of chorionic villi, apoptosis of infected cells by direct viral damage, inhibition of mitosis, and restricted development of precursor cells by the virus, and cytopathic damage to endothelial cells of blood vessels resulting in ischemia of developing organs.

• #3 Rubella – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/rubella/symptoms-causes/syc-20377310

  Rubella is caused by a virus that’s passed from person to person. It can spread when an infected person coughs or sneezes. It can also spread by direct contact with infected mucus from the nose and throat. It can also be passed on from pregnant women to their unborn children through the bloodstream. […] A person who has been infected with the virus that causes rubella is contagious for about one week before the onset of the rash until about one week after the rash disappears. An infected person can spread the illness before the person realizes he or she has it. […] However, if you’re pregnant when you get rubella, the effect on your unborn child may be severe, and in some cases, fatal. Up to 90% of infants born to mothers who had rubella during the first 12 weeks of pregnancy develop congenital rubella syndrome. This syndrome can cause one or more problems, including: Growth delays, Cataracts, Deafness, Problems with the development of the heart (congenital heart defects), Problems with the development of other organs, Problems with mental development and learning. […] The highest risk to the fetus is during the first trimester, but exposure later in pregnancy also is dangerous.

• #3 4 Measles, Mumps, and Rubella Vaccine | Adverse Effects of Vaccines: Evidence and Causality | The National Academies Press

  https://nap.nationalacademies.org/read/13164/chapter/6

  Rubella virus infection during pregnancy can lead to congenital rubella infection in neonates. The disease outcome is directly correlated to the age of the fetus at the time of infection, with younger fetuses experiencing more severe disease. Infections within the first 2 months of pregnancy can cause multiple congenital defects or spontaneous abortion in 65 to 85 percent of women. Infections in the third month and fourth month are associated with a single defect in 30 to 35 percent and 10 percent of cases, respectively. Commonly associated defects include transient thrombocytopenia purpura and meningoencephalitis, as well as permanent and developmental manifestations such as hearing loss, pulmonic stenosis, mental retardation, and behavioral disorders. Other less common manifestations include myocardial abnormalities, hepatitis, and seizure disorders. Studies have also shown that diabetes mellitus occurs 50 times more frequently in children with congenital rubella, and insulin-dependent diabetes has been reported in 40 percent of adults who were congenitally infected with rubella during the 1942 rubella epidemic.

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