YALE JOURNAL OF BIOLOGY AND MEDICINE 82 (2009), pp.153-159. Copyright © 2009. MINI-REVIEW Tasleem Samji Influenza A: Understanding the Viral Life Cycle Graduate student, Department of Microbiology, Yale University School of Medicine, New Haven. Connecticut Influenza A virus belongs to the family of Orthomyxoviridae. It is an enveloped virus with a negative sense RNA segmented genome that encodes for 11 viral genes. This virus has evolved a number of mechanisms that enable it to invade host cells and subvert the host cell machinery for its own purpose, that is, for the sole production of more virus. Two of the mechanisms that the virus uses are “cap-snatching” and preventing the host cell from ex- pressing its own genes. This mini-review provides a brief overview as to how the virus is able to invade host cells, replicate itself, and exit the host cell. Influenza A belongs to the family of F2) [1]. INTRODUCTION Orthomyxoviridae. It is an enveloped virus with a genome made up of negative sense, single-stranded, segmented RNA. The In- fluenza A viruses have eight segments that encode for the 11 viral genes: hemagglu- tinin (HA†), neuraminidase (NA), matrix 1 (M1), matrix 2 (M2), nucleoprotein (NP), non-structural protein 1 (NSP1), non-struc- tural protein 2 (NS2; also known as nuclear export protein, NEP), polymerase acidic protein (PA), polymerase basic protein 1 (PB1), polymerase basic protein 2 (PB2) and polymerase basic protein 1 – F2 (PB1- The influenza virus virions are known to display a number of shapes, with the most abundant one being roughly spheri- cal. The viral envelope is made up of a lipid bilayer that contains three of the viral transmembrane proteins: HA, NA, and M2. This lipid bilayer is derived from the host’s plasma membrane and is known to contain both cholesterol-enriched lipid rafts and non-raft lipids [2-4]. HA is the most abundant envelope protein at approx- imately 80 percent, followed by NA, To whom all correspondence should be addressed: Tasleem Samji, Department of Micro- biology, Yale University School of Medicine, New Haven. Connecticut; E-mail: tasleem.samji@yale.edu. †Abbreviations: HA, hemagglutinin; NA, neuraminidase; M1; matrix 1; M2, matrix 2; NP, nucleoprotein; NSP1, non-structural protein 1; NS2, non-structural protein 2; NEP, nuclear export protein; PA, polymerase acidic protein; PB1, polymerase basic protein 1; PB2, polymerase basic protein 2; PB1-F2, polymerase basic protein 1 – F2; vRNPs, viral ri- bonucleoproteins; Pol II, Cellular RNA Polymerase II; CTD, C-terminal repeat domain; snRNAs, small nuclear RNAs; NS1-BP, NS1 binding protein; AAUAAA, polyadenylation signal; CPSF, cleavage and polyadenylation specificity factor; PABPII, poly(A) binding protein II; RdRp, RNA dependent RNA polymerase; mRNAs, messenger RNAs. Keywords:Influenza A; virus; cap-snatching; host shut off; sialic acid; hemagglutinin; HA; NA; PB1; PB2; PA; M2; M1; NP; PB1-F2; NEP; NS1; NS2 153