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Scheme of Influenza A virus replication

An influenza A virion is composed of the nucleocapsid, a surrounding layer of the matrix protein (M1) and the membrane envelope. The envelope contains two major surface glycoproteins, i.e. hemagglutinin (HA) and neuraminidase (NA), and a minor membrane protein M2. The nucleocapsid consists of individual ribonucleoproteins (vRNPs). Each vRNP contains one of the 8 genomic negative sense RNA segments (vRNA), multiple copies of the major structural protein NP and a few copies of the RNA dependent-RNA-polymerase complex (not shown). All 8 vRNA species must be present in an infectious virion.

A virion attaches to the host cell membrane via HA and enters the cytoplasm by receptor-mediated endocytosis (STEP 1), thereby forming an endosome. A cellular trypsin-like enzyme cleaves HA into products HA1 and HA2 (not shown). HA2 promotes fusion of the virus envelope and the endosome membranes. A minor virus envelope protein M2 acts as a ion channel thereby making the inside of the virion more acidic. As a result, the major envelope protein M1 dissociates from the nucleocapsid and vRNPs are translocated into the nucleus (STEP 2) via interaction between NP and cellular transport machinery. In the nucleus, the viral polymerase complexes transcribe (STEP 3a) and replicate (STEP 3b) the vRNAs. Newly synthesized mRNAs migrate to cytoplasm (STEP 4) where they are translated. Posttranslational processing of HA, NA, and M2 includes transportation via Golgi apparatus to the cell membrane (STEP 5b). NP, M1, NS1 (nonstructural regulatory protein - not shown) and NEP (nuclear export protein, a minor virion component - not shown) move to the nucleus (STEP 5a) where bind freshly synthesized copies of vRNAs. The newly formed nucleocapsids migrate into the cytoplasm in a NEP-dependent process and eventually interact via M1 with a region of the cell membrane where HA, NA and M2 have been inserted (STEP 6). Then the newly synthesized virions bud from infected cell (STEP 7). NA destroys the sialic acid moiety of cellular receptors, thereby releasing the progeny virions.

Although influenza viruses have been extensively studied for years, some aspects of their replication (especially morphogenesis) remain poorly understood.

Influenza A virus genome