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it's just that it seems every week there is a post with misunderstandings on how the virus works and no one listens to the DU scientists who try to explain it. i'm by no means an expert (just a grad student working on the genetics and molecular bio of how influenza jumps the species barrier). and, of course, there *could* be a pandemic of a HPAI virus, as that has happened in the past. but here are my $0.02 cents (which is really more like $100,000 as that's what this damn graduate education is costing me). if you will forgive me, i've mostly copied and pasted from one of my papers on the subject. so, here's a (LONG) synopsis:
Historical and emerging influenza: Potential human influenza pandemics have been described for over 2400 years, although it is widely agreed upon that the first real pandemic occurred in 1580 (Potter 2001). Since then major pandemics arise about every 10-40 years from viruses mainly of Asian origin (Hampson and Mackenzie 2006). The most devastating worldwide outbreak of influenza in recent history was the pandemic of 1918, where it is estimated 50 million people died and 25% of the world’s population was inflicted with disease (Potter 2001). Fortunately, influenza pandemics are relatively rare, although epidemics occur frequently. For example, this current flu season (2007-2008) has suffered a higher than usual number of influenza cases due to insufficient immunity imparted by the currently administered vaccine (CDC 2008).
Influenza virus has been isolated in many species, including birds (Slemons 1974), seals (Geraci et al. 1982), whales (Hinshaw et al. 1986), horses (Sovinova et al. 1958), pigs (Shope 1931), and dogs (Crawford et al. 2005). As seen in the 1918 and 1957 pandemics, influenza viruses that switch from one species to another are often more virulent in naïve hosts. There has been much concern recently that a human influenza pandemic could transpire if a particularly virulent form of avian influenza endemic in waterfowl suddenly jumps the species barrier – not only infecting humans, but also mutating into a strain that can be transmitted among humans. In 1997, a high pathogenic avian influenza (HPAI) H5N1 virus was isolated from influenza-infected humans in Hong Kong (de Jong et al. 1997), and has since been observed in other patients throughout Asia (Beigel et al. 2005; WHO 2008). Although there are few cases of H5N1 being transmitted among humans, the virus has been fatal in >60% of cases reported to the World Heath Organization since 2003 (WHO, 2008). Due to the high death rate of H5N1, transmission of influenza strains between and among species is currently a major focus of influenza research.
Antigenic drift and antigenic shift: As a member of the Orthomyxoviridae family, influenza A is a negative-sense, ssRNA virus with a genome consisting of eight segments. Influenza has been evolutionarily successful partly because of mutations inherent in RNA error-prone replication. Two of the segments, the HA (haemagglutinin) and NA (neuraminidase) genes, play particular roles in influenza species specificity (reviewed in Landholt and Olsen 2007); there are 16 known HAs and 9 known NAs, which have all been identified in avian flu strains. Single amino acid changes in HA and/or NA resulting from host selection pressures lead to newly circulating viruses that may cause regional epidemics; thus, antigenic drift. Antigenic shift, on the other hand, is a much more dramatic mutation of the influenza genome and may lead to pandemics. There are two possible ways for antigenic shift to occur: (1) reassortment of avian- and human-like viral segments in a “mixing vessel” where entire segments can be replaced by the same segments from another strain, or (2) adaptation of an avian-like virus to a human-like virus in a host (Karasin et al. 2000). In both cases, a host must be able to be infected with both avian- and human-like viruses. Japanese quail (Wan and Perez 2005) and pigs (Landholt et al. 2003) have been shown to fit this host model for generation of pandemic viruses. Of course, other factors contribute to epidemics and pandemics such as the ability of the virus to be transmitted among humans, the number of susceptible hosts, and the extent of antigenic variation in mutated influenza strains.
Receptor biology: Influenza infection requires, like all pathogens, uptake by a host cell before it can be translated and replicated. Attachment and binding to cellular receptors depends on the type of sialic acid linkage to the oligosaccharide receptor attached to the host cell surface. Generally, avian-like influenza viruses have a higher affinity to sialic acid receptors that have α-2,3 linkages to the penultimate sugar on oligosaccharides, whereas human-like viruses bind to α-2,6 linkages with greater affinity (Matrosovich et al. 1997). In antigenic drift, a single mutation in the amino acid sequence of the HA gene may allow a particular strain to have greater affinity to the sialic acid receptors. In antigenic shift, a whole HA gene from one strain of influenza may be completely replaced by the HA gene from another strain, or the strain may develop affinity to a different sialic acid linkage receptor, rendering the virus able to affect new species. Pigs and Japanese quails have both types of sialic acid linkages (Gambaryan et al. 2005; Wan and Perez 2005), which is partly why both species can become infected with both avian- and human-like influenza viruses.
IN SUMMARY: Avian influenza viruses are found worldwide - most are the low path variety. Yes, there are HPAIs that are a cause for concern, but they are also naturally found in waterfowl. It is not inconceivable that these newly found HPAIs are from migrants bird that usually show no signs of infection or from illegally transported birds. HPAI is serious - but a lot has to happen (both to the virus and to the host) to make it a major everyday concern.
pm me if you want any particular refs - i've gone on long enough...
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