- Molecular Structure
- Genetic Change
- Subtype H5N1
- Organizations' Roles
- Current Research
Molecular Structure of Influenzavirus A
Subtypes are labeled according to the categories of two main surface glycoproteins located on the surface of the viral capsid: H number (for hemagluttinin) and N number (for neuraminidase), with numbers being given in ascending order based on the date that the subtype was discovered. There are currently 16 HA (hemagluttinin) and 9 NA (neuraminidase) types known. Major changes to the shapes of the hemagluttinin and neuraminidase result in changes in the ability to infect or transmit, thus changing the species the virus is capable of infecting.
The influenzavirus A genome consists of 10 genes coded in RNA whose lengths vary per strain and substrain. In fact, the viral genes being studied have shown signs of having been in constant fluctuation since introduction to human populations. Specific methods of recombination between influenzavirus capable infecting two species are unknown, and some research has been targeted in this specific direction.
Avian flu viruses’ genome consists of 10 genes coded in RNA whose lengths vary per strain and substrain. In fact, the IVA genes being studied have shown signs of having been in constant fluctuation since introduction to human populations. Specific methods of recombination between IVA infecting two species are unknown, and some research has been targeted in this specific direction.
Genetic Change of Influenzavirus A
One primary danger that influenzavirus A poses is its ability to mutate and adapt rapidly to new environments and hosts. These changes are brought about by genetic changes, which allow for novel methods of infection and thus the ability to jump to species that were previously unaffected by the virus. Influenzavirus A genetic changes can be broadly categorized into two types: antigenic drift and antigenic shift. Antigenic drift applies to the random genetic mutations that occur through point mutations, or single accidental mutations that occur through chance misfunctions in the replication of the viral genome. Antigenic shift applies to sudden, major changes in the genome that typically result in a new subtype of influenzavirus.
Of primary concern for researchers is the ability of the influenzavirus A to acquire the capability to infect humans in addition to birds. Since influenzavirus strains endemic to wild fowl are typically only capable of infecting other birds due to their specific capsid protein structures, specific changes to the amino acid chains that compose the capsid proteins are necessary to allow for the jump across the species barrier. According to research by the CDC, influenzavirus can gain increased transmissibility to humans by two main methods: reassortment and gradual mutation.
Reassortment in this case is a kind of antigenic shift, as described above, in which human and avian viruses encounter each other in a single host and exchange genetic material, allowing for genes that promote human infection to be transferred to the influenzavirus AŐs genome. Of note is the fact that the host in question does not need to be human or avian; in some cases, an intermediary host species, such as pigs, can allow for this cross-species intermingling of viruses. Reassortment is dangerous in that the change in human transmission rates would generally be extremely dramatic, posing the threat of a severe pandemic with little or no warning, given the random nature of reassortmentŐs occurrence.
Gradual mutation is a kind of antigenic drift, in which a single strain of virus makes a chance infection of a human host without having well-adapted proteins for repeated transmission. While the virus infects the host, it mutates as certain random mutations during the process of viral multiplication allow for greater pathogenicity. This increased ŇfitnessÓ of the changing virus strains promotes transmission to other humans, where the process is repeated. Eventually, this leads to a greatly promoted capability of human infection. Gradual mutation is more predictable and somewhat easier to detect, since early warning signs will be given by index cases of the flu followed by increasing numbers of cases in the immediate vicinity of the index case.
Subtype H5N1 is a HPAI that is capable of crossing the species barrier to infect humans, although has not reached human-to-human transmission. This is currently being carefully monitored and combated, due to the danger of it poses as a possible pandemic virus.
H5N1 is resistant to amantadine and rimantadine. Oseltamavir and zanamavir may be effective in treatment, although this has not been demonstrated.
The fight against avian flu is one that is worldwide, and national and international health agencies play a major role. The United StatesŐs Centers for Disease Control (CDC) is tasked with tracking and combating the spread of avian flu. The National Institutes of Health (NIH) works in conjunction with the Department of Homeland Security and the Federal Emergency Management Agency (FEMA) in order to develop national response policies to the occurrence of an avian flu epidemic in the US. The international public health group World Health Organization (WHO) also sponsors and coordinates research and initiatives in the hopes of preventing an avian flu pandemic.
Information About Current Research
The original H1N1 strain and all other known human-contagious strains of IVA are classified as biosafety level four (BSL-4) pathogens. As such, there are currently only 16 laboratories in the world with the security and safety measures necessary for the controlled environment required to perform research without putting any researchers at risk. U.S. researchers may apply to receive samples of influenzavirus A or sequences of the virus RNA, although they must be supervised at one of the U.S.-regulated laboratories.