H5N1 Influenza A: Difference between revisions
No edit summary |
No edit summary |
||
| Line 31: | Line 31: | ||
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare (5). | The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare (5). | ||
===<i>Virulence Factors</i>=== | |||
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versos low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission. | |||
==Clinical features== | ==Clinical features== | ||
Revision as of 13:19, 23 July 2013
Etiology/Bacteriology
Taxonomy
| Domain = Viruses
| Class = ssRNA viruses
| Order = ssRNA negative strand viruses
| Family = Orthomyxoviridae
| Genus = Influenzavirus A
| species = Influenza A virus
|
NCBI: [1] Genome: Influenza A Virus H5N1 [2] |
Description
Avian Influenza A (H5N1) is a type of influenza virus responsible for causing severe respiratory disease in birds, generally waterfowl and humans. However, researchers have yet to definitively document human-to-human transmission and victims of avian-to-human transmission generally spend substantial amounts of time around birds (like poultry farm workers, migratory duck herders, etc.) There is a growing amount of concern about the virus because of its high mortality rate and its disposition to mutation, which renders the human adaptive immune response fairly limited and the virus would be devastating if it were to mutate to a strain capable of human-to-human transmission. Symptoms of infection include high fever (>38°C), malaise, cough, sore throat, muscle aches, abdominal or chest pain, and diarrhea. The sequelae of H5N1 infection are often severe respiratory illness including pneumonia and acute respiratory distress syndrome as well as neurological changes like altered mental state and seizures. Treatment often involves implementation of the antiviral medication oseltamivir. At this stage, all vaccinations are still experimental (3).
Pathogenesis
Transmission
Transmission of H5N1 primarily occurs via direct avian-to-human contact. Major risk factors include handling diseased poultry and the consumption of raw or undercooked poultry products. The exact mode and sites of infection in the respiratory tract remain unknown. H5N1 also has several mammalian hosts including cats, dogs, and ferrets. None have been shown to transmit the disease to humans. However, a genetically modified strain of the virus was capable of airborne transmission in ferrets, which gives insight into the possibility of human-to-human transmission (4). The mode of transmission remains unclear for about one quarter of infected patients and environment-to-human transmission has not been ruled out. It is still uncertain whether infection can begin in the gastrointestinal tract, but it has been implicated in other mammals and is an open area of research.
Infectious Dose, Incubation, and Epidemiology
Infectious Dose
There is not an agreed upon infectious dose for H5N1 and it is likely dependent on a number of host factors like age, race, genes, and location. However, it seems clear that a low number of viral particles can proliferate extremely successfully once they have become bound in the respiratory tract.
Incubation
The incubation period for H5N1 infection is generally 7 days or less, many times as little as 2-5 days. In cases where human-to-human transmission likely occurred the average is 3 days. However, some reports estimate as long as 8-9 days.
Epidemiology
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare (5).
Virulence Factors
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versos low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission.
Clinical features
Diagnosis
Treatment
Prevention
Host Immune Response
References
References
Created by {Marrett Hild}, students of Tyrrell Conway at the University of Oklahoma.
