|
| ||||||||
| ||||||||
|
Biosecurity BriefingStudy Suggests H7 Avian Influenza Viruses are Developing Greater Ability to Infect Humans By Matthew Watson, June 6, 2008 On May 27, 2008, the Proceedings of the National Academy of Sciences (PNAS) published a study by Belser and colleagues which provides evidence that a recent H7 strain of avian influenza A virus has acquired a trait which could allow for increased disease transmission among humans.1 At the cellular level, the ability for a virus to cause disease is partially controlled by how strongly the virus is able to bind to sialic acid (SA) receptors that are present on the surface of a host cell. These receptors vary in both type and anatomic location. Birds have α2-3 type SA receptors in their guts, whereas humans have α2-6 type SA receptors in their respiratory tracts. Viruses adapted to attach well to one type of SA receptor generally cannot attach well to the other.1 Since 2002, H7 strains have been causing both highly pathogenic (HPAI) and low pathogenic (LPAI) avian influenza outbreaks in poultry in North America and Eurasia. Isolated human infections have been reported in British Columbia (HPAI H7N3, 2004),2 the United Kingdom (LPAI H7N2, 2007)3 and New York (LPAI H7N2, 2003). In 2003, an epidemic of HPAI H7N7 took place at a poultry farm in the Netherlands, which produced over 80 human cases and one death.4 In contrast to H5N1, which attacks the respiratory tract, almost all the human cases of H7 infection have been manifested as conjunctivitis (eye infection).1 Presumably, this is related to high concentrations of α2-3 SA receptors in human conjunctiva. This study analyzed the affinity, or strength, to which nine H7 strains bound to the human α2-6 SA receptors, and found that four recent North American H7 strains showed an increased affinity for these receptors. Further, when researchers inoculated ferrets (an animal model with receptors similar to humans) with an H7 influenza strain (NY/107) isolated from a New York man infected in 2003, they observed transmission by direct contact between infected and uninfected animals. This phenomenon was not noted with any other viral strain.1 The authors conclude that the adaptation of viral attachment sites to the human respiratory tract may be an essential step in the evolution of a pandemic virus. This paper provides evidence that such adaptation has occurred among some North American H7 viruses and at least one H7 strain has acquired the capability to be transmitted efficiently between ferrets. To date, the H5N1 avian influenza has not evolved in this way.1 The article suggests that increased disease surveillance and clinical vigilance are needed to rapidly identify further evidence of viral evolution. Additionally, these results may have significant implications for pre-pandemic influenza vaccine development, as it is unclear whether either seasonal or HPAI H5N1 vaccines currently in development would provide cross protective immunity against an H7 virus. This finding makes the need for “broad spectrum” influenza vaccines more apparent. Research in this area is ongoing at the National Institutes of Health (NIH).5 It is also worth mentioning that no further cases of human NY/107, or any other human outbreaks of H7 avian influenza have been reported since 2004. References
|