Location on the evolutionary trees of the non-structural protein (NS) and neuraminidase (NA) genes of late human influenza A (H2N2) viruses: parental viruses of the NS and NA genes of Hong Kong influenza A (H3N2) viruses

Nakao, Haruhisa; Nakajima, Kazuki; Nakajima, Setsuko

doi:10.1099/0022-1317-74-8-1667

Cited by 13 publications

(14 citation statements)

References 30 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar to the HA gene, the NA gene of late H2N2 viruses formed two distinct clades, I and II (Fig. 1b), confirming previous analysis [5]. All NA genes of H3N2 viruses of 1968 formed a cluster near H2N2 viruses of clade I, suggesting that H2N2 viruses of clade I were the contributing ancestral viruses of human H3N2 viruses.…”

Section: Methodssupporting

confidence: 88%

Evolutionary analysis of human H2N2 and early H3N2 influenza viruses: evidence for genetic divergence and multiple reassortment among H2N2 and/or H3N2 viruses

Lindstrom

Cox

Klimov

2004

International Congress Series

View full text Add to dashboard Cite

Section: Methodssupporting

confidence: 88%

Evolutionary analysis of human H2N2 and early H3N2 influenza viruses: evidence for genetic divergence and multiple reassortment among H2N2 and/or H3N2 viruses

Lindstrom

Cox

Klimov

2004

International Congress Series

View full text Add to dashboard Cite

“…There is a scant amount of molecular data on the evolution of the 1918 H1N1 strain during its first decade 38, 39. Although extensive phylogenetic analysis of the H2N2 1957 pandemic strain lineage revealed that the original strain diverged into two distinct co-circulating clades within 8– 10 years of its introduction, it has not shown that any of these changes occurred in 1957–1958 40, 41. Given that the 2009 H1N1 virus received nearly all of its genes (except PB1) from viruses of recent non-human origin, it would not be surprising to see evolutionary rates exceeding those observed for seasonal H3N2 and H1N1 42, 43.…”

Section: Discussionmentioning

confidence: 99%

Vaccination Deep Into a Pandemic Wave

Lee

Brown

Cooley

et al. 2010

American Journal of Preventive Medicine

View full text Add to dashboard Cite

Background In December 2009, when the H1N1 influenza pandemic appeared to be subsiding, public health officials and unvaccinated individuals faced the question of whether continued H1N1 immunization was still worthwhile. Purpose To delineate what combinations of possible mechanisms could generate a third pandemic wave and then explore whether vaccinating the population at different rates and times would mitigate the wave. Methods As part of ongoing work with the Office of the Assistant Secretary of Preparedness and Response at the USDHHS during the H1N1 influenza pandemic, the University of Pittsburgh Models of Infectious Disease Agents Study team employed an agent-based computer simulation model of the Washington, DC metropolitan region to delineate what mechanisms could generate a “third pandemic wave” and explored whether vaccinating the population at different rates and times would mitigate the wave. This model included explicit representations of the region's individuals, school systems, workplaces/commutes, households, and communities. Results Three mechanisms were identified that could cause a pandemic third wave: substantially increased viral transmissibility from seasonal forcing (changing influenza transmission with changing environmental conditions, i.e., seasons) and progressive viral adaptation, an immune escape variant, and changes in social mixing from holiday school closures. Implementing vaccination for these mechanisms even during the down-slope of the fall epidemic wave significantly mitigated the third wave. Scenarios showed the gains from initiating vaccination earlier, increasing the speed of vaccination, and prioritizing population subgroups based on Advisory Committee on Immunization Practices recommendations. Conclusions Additional waves in an epidemic can be mitigated by vaccination even when an epidemic appears to be waning.

show abstract

“…In 1968, Hong Kong Flu emerged by genetic introduction of the H3 HA gene from avian virus to H2N2 human seasonal virus that originated from 1957 Asian Flu. 65) At that time, the viral RNA polymerase subunit PB1 gene of 1968 Hong Kong Flu was reported to be inherited from that of avian virus. 66) We found that NAs of H2N2 human seasonal viruses in 1968 could be divided into two types, low-pH-stable NA and lowpH-unstable NA types.…”

Section: Analysis Of Pandemic Occurrence In View Of the Low-ph Stabilmentioning

confidence: 99%

Low-pH Stability of Influenza A Virus Sialidase Contributing to Virus Replication and Pandemic

Takahashi

Suzuki

2015

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The spike glycoprotein neuraminidase (NA) of influenza A virus (IAV) has sialidase activity that cleaves the terminal sialic acids (viral receptors) from oligosaccharide chains of glycoconjugates. A new antigenicity of viral surface glycoproteins for humans has pandemic potential. We found "low-pH stability of sialidase activity" in NA. The low-pH stability can maintain sialidase activity under acidic conditions of pH 4-5. For human IAVs, NAs of all pandemic viruses were low-pH-stable, whereas those of almost all human seasonal viruses were not. The low-pH stability was dependent on amino acid residues near the active site, the calcium ion-binding site, and the subunit interfaces of the NA homotetramer, suggesting effects of the active site and the homotetramer on structural stability. IAVs with the low-pH-stable NA showed much higher virus replication rates than those of IAVs with low-pH-unstable NA, which was correlated with maintenance of sialidase activity under an endocytic pathway of the viral cell entry mechanism, indicating contribution of low-pH stability to high replication rates of pandemic viruses. The low-pH-stable NA of the 1968 H3N2 pandemic virus was derived from the low-pH-stable NA of H2N2 human seasonal virus, one of two types classified by both low-pH stability in N2 NA and a phylogenetic tree of N2 NA genes. The 2009 H1N1 pandemic virus acquired low-pH-stable NA by two amino acid substitutions at the early stage of the 2009 pandemic. It is thought that low-pH stability contributes to infection spread in a pandemic through enhancement of virus replication.

show abstract

Location on the evolutionary trees of the non-structural protein (NS) and neuraminidase (NA) genes of late human influenza A (H2N2) viruses: parental viruses of the NS and NA genes of Hong Kong influenza A (H3N2) viruses

Cited by 13 publications

References 30 publications

Evolutionary analysis of human H2N2 and early H3N2 influenza viruses: evidence for genetic divergence and multiple reassortment among H2N2 and/or H3N2 viruses

Evolutionary analysis of human H2N2 and early H3N2 influenza viruses: evidence for genetic divergence and multiple reassortment among H2N2 and/or H3N2 viruses

Vaccination Deep Into a Pandemic Wave

Low-pH Stability of Influenza A Virus Sialidase Contributing to Virus Replication and Pandemic

Contact Info

Product

Resources

About