Tuesday, 28 May 2013

H7N9: airborne transmission not at pandemic levels - infects upper & lower airways, lymph nodes and brain in ferrets.

In a collaborative effort published last week in Science, researchers from China, Canada and the US infected ferrets with a human H7N9 isolate (A/Shanghai/2/2013; "SH2"). The aim was to understand infection, transmission and pathogenicity due to the virus in the main mammalian model for such studies.

Ferrets showed upper respiratory tract disease, similar to that due to influenza A(H1N1)pdm 2009 virus infection, with shedding beginning the day after nasal inoculation - preceding any signs of disease. Obvious ramifications for stealthy spread of virus in this prodromal phase

Infected ferrets housed in the same cage as a non-infected ferret (introduced 24-hours after the the infection of the first occupants) easily transmitted SH2 to the newcomer who showed signs of illness within 36-hours; the same time at which lung inflammation and virus replication in nasal, tracheal, bronchiolar, lymph node and brain tissues was occurring. All these ferrets produced a diagnostic rise in antibodies by 14 days (They seroconverted).

An uninfected ferret in a downwind cage, separated by 10cm, acquired and shed SH2 at 36-hours after exposure (1 animal in 3 experiments). This ferret and one other seroconverted at 14 days post-exposure.

Airborne transmission was therefore possible in two-thirds of exposures in these experiments. H1N1pdm 2009 infected ferrets all shed virus regardless of route of infection confirming practically that H7N9 has some way to go to spread on a par with a known pandemic influenza virus.

Pigs also supported H7N9 infection showing signs and symptoms of disease 0.5 days after virus load was measurable. Direct contact H7N9 transmission was possible with an antibody rise occurring in 25% (1 of 4) of pigs but no virus shedding. No airborne transmission was detectable in the pigs. H1N1pdm 2009 virus was spread efficiently by direct and airborne routes in pigs.

Perhaps pigs are not the universal intermediary mixing vessel they are made out to be - being more susceptible to humanised influenza viruses than those closer to their avian hosts?