Nearly Complete Genome Sequence of Human Influenza Virus Strain A/Almaty/6327/2014 (H1N1) from Central Asia

An influenza virus strain, A/Almaty/6327/2014 (H1N1), was isolated in Almaty (in southeastern Kazakhstan) during a human population surveillance study in 2014. Here, we present the nearly complete genome sequence of this epidemic strain that was compared to the postpandemic variants of A(H1N1)pdm09.

IFITM3 protects the heart during influenza virus infection

Influenza virus can disseminate from the lungs to the heart in severe infections and can induce cardiac pathology, but this has been difficult to study due to a lack of small animal models. In humans, polymorphisms in the gene encoding the antiviral restriction factor IFN-induced transmembrane protein 3 (IFITM3) are associated with susceptibility to severe influenza, but whether IFITM3 deficiencies contribute to cardiac dysfunction during infection is unclear. We show that IFITM3 deficiency in a new knockout (KO) mouse model increases weight loss and mortality following influenza virus infections. We investigated this enhanced pathogenesis with the A/PR/8/34 (H1N1) (PR8) influenza virus strain, which is lethal in KO mice even at low doses, and observed increased replication of virus in the lungs, spleens, and hearts of KO mice compared with wild-type (WT) mice. Infected IFITM3 KO mice developed aberrant cardiac electrical activity, including decreased heart rate and irregular, arrhythmic RR (interbeat) intervals, whereas WT mice exhibited a mild decrease in heart rate without irregular RR intervals. Cardiac electrical dysfunction in PR8-infected KO mice was accompanied by increased activation of fibrotic pathways and fibrotic lesions in the heart. Infection with a sublethal dose of a less virulent influenza virus strain (A/WSN/33 [H1N1]) resulted in a milder cardiac electrical dysfunction in KO mice that subsided as the mice recovered. Our findings reveal an essential role for IFITM3 in limiting influenza virus replication and pathogenesis in heart tissue and establish IFITM3 KO mice as a powerful model for studying mild and severe influenza virus-induced cardiac dysfunction.

Genome Sequences of an H9N2 Avian Influenza Virus Strain Found in Pakistan in 2017

In 2017, we isolated an H9N2 avian influenza virus in Pakistan. Genetic analysis showed that the A/chicken/Kasoor/SI36/2017(H9N2) isolate belongs to the G1 lineage. In addition, this isolate possesses mammalian host-specific mutations which could possibly favor interspecies transmission, suggesting that Pakistani H9N2 viruses are still potentially infectious for mammals.

Near-Complete Genome Sequence of Avian Influenza Virus Strain A/mallard/Balkhash/6304/2014 (H1N1) from Kazakhstan

An avian influenza virus strain, A/mallard/Balkhash/6304/2014 (H1N1), was isolated during a wild bird monitoring study in Kazakhstan in 2014. The virus was isolated from a wild mallard duck (Anas platyrhynchos) in eastern Kazakhstan.

A fluorogenic 2D glycosheet for the simultaneous identification of human- and avian-receptor specificity in influenza viruses

A duplexed 2D glycosheet has been developed for the simultaneous identification of the dual receptor specificity of a single influenza virus strain in a homogeneous solution.

Protective Efficacy of the Conserved NP, PB1, and M1 Proteins as Immunogens in DNA- and Vaccinia Virus-Based Universal Influenza A Virus Vaccines in Mice

ABSTRACTThe conventional hemagglutinin (HA)- and neuraminidase (NA)-based influenza vaccines need to be updated most years and are ineffective if the glycoprotein HA of the vaccine strains is a mismatch with that of the epidemic strain. Universal vaccines targeting conserved viral components might provide cross-protection and thus complement and improve conventional vaccines. In this study, we generated DNA plasmids and recombinant vaccinia viruses expressing the conserved proteins nucleoprotein (NP), polymerase basic 1 (PB1), and matrix 1 (M1) from influenza virus strain A/Beijing/30/95 (H3N2). BALB/c mice were immunized intramuscularly with a single vaccine based on NP, PB1, or M1 alone or a combination vaccine based on all three antigens and were then challenged with lethal doses of the heterologous influenza virus strain A/PR/8/34 (H1N1). Vaccines based on NP, PB1, and M1 provided complete or partial protection against challenge with 1.7 50% lethal dose (LD50) of PR8 in mice. Of the three antigens, NP-based vaccines induced protection against 5 LD50and 10 LD50and thus exhibited the greatest protective effect. Universal influenza vaccines based on the combination of NP, PB1, and M1 induced a strong immune response and thus might be an alternative approach to addressing future influenza virus pandemics.