tetano
Editor, Senior Moderator
Published ahead of print 21 August 2013, doi: 10.1128/JVI.01544-13 JVI.01544-13
Fecal influenza in mammals: selection of novel variants
Zeynep A. Ko?era,
John Obenauerb,
Hassan Zaraketa,
Jinghui Zhangb,
Jerold E. Rehgc,
Charles J. Russella and
Robert G. Webstera#
+ Author Affiliations
Departments of aInfectious Diseases-Division of Virology
bComputational Biology
cPathology, St Jude Children?s Research Hospital, Memphis, TN 38105-3678, USA
ABSTRACT
In aquatic birds, influenza A viruses mainly replicate in the intestinal tract without significantly affecting the health of the host, but in mammals they replicate in the respiratory tract and often cause disease. Occasionally, influenza viruses have been detected in stool samples of hospitalized patients and in rectal swabs of naturally or experimentally infected mammals. In this study, we compared the biological and molecular differences among four wild-type avian H1N1 influenza viruses and their corresponding fecal and lung isolates in DBA/2J and BALB/cJ mice. All fecal and lung isolates were more pathogenic than the original wild-type viruses, when inoculated into mice of both strains. The increased virulence was associated with the acquisition of genetic mutations. Most of the novel genotypes emerged as PB2E627K or HAF128V, F454L, or H300P variants, and double-mutants frequently occurred in the same isolate. However, influenza strain- and host-specific differences were also observed in terms of selected variants. The avian H1N1 virus of shorebird origin appeared to be unique in its ability to rapidly adapt to BALB/cJ mice via the fecal route, compared to the adaptability of the H1N1 virus of mallard origin. Furthermore, bimodal distribution was observed in fecal shedding in mice infected with the fecal isolates, while normal distribution was observed after infection with the lung isolates or wild-type virus. Fecal isolates contained HA mutations that increased the activation pH of the HA protein. We conclude that influenza variants that emerge in fecal isolates in mammals might influence viral transmission, adaptation to mammals, and viral ecology or evolution.
http://jvi.asm.org/content/early/2013/08/16/JVI.01544-13.abstract
Fecal influenza in mammals: selection of novel variants
Zeynep A. Ko?era,
John Obenauerb,
Hassan Zaraketa,
Jinghui Zhangb,
Jerold E. Rehgc,
Charles J. Russella and
Robert G. Webstera#
+ Author Affiliations
Departments of aInfectious Diseases-Division of Virology
bComputational Biology
cPathology, St Jude Children?s Research Hospital, Memphis, TN 38105-3678, USA
ABSTRACT
In aquatic birds, influenza A viruses mainly replicate in the intestinal tract without significantly affecting the health of the host, but in mammals they replicate in the respiratory tract and often cause disease. Occasionally, influenza viruses have been detected in stool samples of hospitalized patients and in rectal swabs of naturally or experimentally infected mammals. In this study, we compared the biological and molecular differences among four wild-type avian H1N1 influenza viruses and their corresponding fecal and lung isolates in DBA/2J and BALB/cJ mice. All fecal and lung isolates were more pathogenic than the original wild-type viruses, when inoculated into mice of both strains. The increased virulence was associated with the acquisition of genetic mutations. Most of the novel genotypes emerged as PB2E627K or HAF128V, F454L, or H300P variants, and double-mutants frequently occurred in the same isolate. However, influenza strain- and host-specific differences were also observed in terms of selected variants. The avian H1N1 virus of shorebird origin appeared to be unique in its ability to rapidly adapt to BALB/cJ mice via the fecal route, compared to the adaptability of the H1N1 virus of mallard origin. Furthermore, bimodal distribution was observed in fecal shedding in mice infected with the fecal isolates, while normal distribution was observed after infection with the lung isolates or wild-type virus. Fecal isolates contained HA mutations that increased the activation pH of the HA protein. We conclude that influenza variants that emerge in fecal isolates in mammals might influence viral transmission, adaptation to mammals, and viral ecology or evolution.
http://jvi.asm.org/content/early/2013/08/16/JVI.01544-13.abstract