Antigenic drift in type A influenza virus: Sequence differences in the hemagglutinin of Hong Kong (H3N2) variants selected with monoclonal hybridoma antibodies

Virology ◽  
1979 ◽  
Vol 98 (1) ◽  
pp. 226-237 ◽  
Author(s):  
W.G. Laver ◽  
G.M. Air ◽  
R.G. Webster ◽  
W. Gerhard ◽  
C.W. Ward ◽  
...  
2010 ◽  
Vol 64 (5-6) ◽  
pp. 307-317
Author(s):  
Bosiljka Djuricic ◽  
Ana Samokovlija ◽  
Zivka Ilic ◽  
Dragan Bacic ◽  
Sonja Radojicic ◽  
...  

The disease caused by Influenza viruses has been well known for a very long time. In the recent period there has been noted an occurrence of pandemics caused by Influenza viruses type A with a high rate of mortality. The ongoing pandemic caused by avian influenza virus serotype H9N9 began in Hong Kong in 1992, and another pandemic caused by serotype H5N1 began in China (Hong Kong) in 1999. The world wide spreading of these viruses occurred due to migratory birds. Avian influenza was confirmed in Serbia in 2007. The goal of this study was to examine whether the avian influenza viruses type A circulate in the region of the Obedska bara marsh, which is a famous resort for many birds in Serbia, as well as many birds migrating from Europe to Africa and vice versa. The samples of blood sera of many animal species (123 samples from fowl, 64 samples from donkeys, 40 samples from horses) were tested by serologic reaction of inhibition of haemmaglutination (IHA) for the presence of antibodies to influenza A subtypes H5N1, H5N2, H5N3, H7N1 and H7N2. Also, the samples of blood sera of experimental chicken exposed to wild life in Obedska bara (sentinel species) were tested. Antibodies to subtypes H5N1, H5N2, H5N3, H7N1 and H7N2 were found in chicken from Dec, Boljevci, Petrovcic and Kupinovo villages but no antibodies were found in blood sera from hams from Dobanovci, Jakovo, Becmen and Surcin villages. From 23 samples from ducks antibodies were detected in 3 samples, and from 22 geese blood sera antibodies were found in 4 samples. From a total of 40 horse blood sera tested one was tested positive, and from 64 donkey sera 17 were positive for the presence of antibodies for avian influenza type A. In blood sera of experimental chicken antibodies were found by subtype H5N1 with corrections with H5N2 and H7N1.


2004 ◽  
Vol 78 (15) ◽  
pp. 8372-8381 ◽  
Author(s):  
Chang-Won Lee ◽  
Dennis A. Senne ◽  
David L. Suarez

ABSTRACT An outbreak of avian influenza (AI) caused by a low-pathogenic H5N2 type A influenza virus began in Mexico in 1993 and several highly pathogenic strains of the virus emerged in 1994-1995. The highly pathogenic virus has not been reported since 1996, but the low-pathogenic virus remains endemic in Mexico and has spread to two adjacent countries, Guatemala and El Salvador. Measures implemented to control the outbreak and eradicate the virus in Mexico have included a widespread vaccination program in effect since 1995. Because this is the first case of long-term use of AI vaccines in poultry, the Mexican lineage virus presented us with a unique opportunity to examine the evolution of type A influenza virus circulating in poultry populations where there was elevated herd immunity due to maternal and active immunity. We analyzed the coding sequence of the HA1 subunit and the NS gene of 52 Mexican lineage viruses that were isolated between 1993 and 2002. Phylogenetic analysis indicated the presence of multiple sublineages of Mexican lineage isolates at the time vaccine was introduced. Further, most of the viruses isolated after the introduction of vaccine belonged to sublineages separate from the vaccine's sublineage. Serologic analysis using hemagglutination inhibition and virus neutralization tests showed major antigenic differences among isolates belonging to the different sublineages. Vaccine protection studies further confirmed the in vitro serologic results indicating that commercial vaccine was not able to prevent virus shedding when chickens were challenged with antigenically different isolates. These findings indicate that multilineage antigenic drift, which has not been observed in AI virus, is occurring in the Mexican lineage AI viruses and the persistence of the virus in the field is likely aided by its large antigenic difference from the vaccine strain.


1981 ◽  
Vol 195 (1) ◽  
pp. 337-340 ◽  
Author(s):  
C W Ward ◽  
T A Dopheide

The relationship between the haemagglutinin from the influenza virus A/duck/Ukraine/1/63 (Hav 7) and the human Hong Kong variants (H3) has been investigated. Amino-acid-sequence analysis shows that the Hav 7 haemagglutinin closely resembles the 1968 human H3 haemagglutinin in structure. However, the number of amino-acid-sequence differences (23) suggest that the Hong Kong haemagglutinin gene did not come directly from A/duck/Ukraine/1/63 but from a virus derived from it by antigenic drift during the period 1963-1968.


1982 ◽  
Vol 136 (4) ◽  
pp. 353-358 ◽  
Author(s):  
JIRO ARIKAWA ◽  
NOBUHISA YAMANE ◽  
KIYOSHI TOTSUKAWA ◽  
NAKAO ISHIDA

1973 ◽  
Vol 71 (4) ◽  
pp. 641-647 ◽  
Author(s):  
D. Hobson ◽  
F. A. Baker ◽  
R. L. Curry ◽  
A. S. Beare ◽  
P. M. O. Massey

Intranasal vaccines of inactivated or living attentuated A2/Hong Kong influenza viruses were compared for clinical acceptability, serological effects and protective efficiency against natural epidemic influenza in a large industrial and clerical population.


2014 ◽  
Vol 59 (4) ◽  
pp. 517-524 ◽  
Author(s):  
B. J. Cowling ◽  
R. A. P. M. Perera ◽  
V. J. Fang ◽  
K.-H. Chan ◽  
W. Wai ◽  
...  

2001 ◽  
Vol 45 (3) ◽  
pp. 749-757 ◽  
Author(s):  
Robert W. Sidwell ◽  
Donald F. Smee ◽  
John H. Huffman ◽  
Dale L. Barnard ◽  
Kevin W. Bailey ◽  
...  

ABSTRACT The cyclopentane influenza virus neuraminidase inhibitor RWJ-270201 was evaluated against influenza A/NWS/33 (H1N1), A/Shangdong/09/93 (H3N2), A/Victoria/3/75 (H3N2), and B/Hong Kong/05/72 virus infections in mice. Treatment was by oral gavage twice daily for 5 days beginning 4 h pre-virus exposure. The influenza virus inhibitor oseltamivir was run in parallel, and ribavirin was included in studies with the A/Shangdong and B/Hong Kong viruses. RWJ-270201 was inhibitory to all infections using doses as low as 1 mg/kg/day. Oseltamivir was generally up to 10-fold less effective than RWJ-270201. Ribavirin was also inhibitory but was less tolerated by the mice at the 75-mg/kg/day dose used. Disease-inhibitory effects included prevention of death, lessening of decline of arterial oxygen saturation, inhibition of lung consolidation, and reduction in lung virus titers. RWJ-270201 and oseltamivir, at doses of 10 and 1 mg/kg/day each, were compared with regard to their effects on daily lung parameters in influenza A/Shangdong/09/93 virus-infected mice. Maximum virus titer inhibition was seen on day 1, with RWJ-270201 exhibiting the greater inhibitory effect, a titer reduction of >104 cell culture 50% infective doses (CCID50)/g. By day 8, the lung virus titers in mice treated with RWJ-270201 had declined to 101.2 CCID50/g, whereas titers from oseltamivir-treated animals were >103CCID50/g. Mean lung consolidation was also higher in the oseltamivir-treated animals on day 8. Both neuraminidase inhibitors were well tolerated by the mice. RWJ-270201 was nontoxic at doses as high as 1,000 mg/kg/day. These data indicate potential for the oral use of RWJ-270201 in the treatment of influenza virus infections in humans.


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