Abstract：
:Adaptation of the prototype A/FM/1/47 H1N1 strain to mice resulted in selection of the A/FM/1/47-MA variant with increased virulence. Earlier analysis identified mutations in the HA and M1 genes that increase virulence in the mouse. Complete sequence analysis identified mutations in the PB1, PB2, HA, NA, and M1 genes. Reassortants were produced between the parental FM and FM-MA strains to obtain viruses that differ due to combinations of mutant genes. To assess the relationship between virulence and replication, the median lethal dose was determined for mice and growth properties were assessed in mouse lung, MDCK cells and chicken embryo. Not only were all five mutations shown to control virulence but also the replicative capacity in the mouse. The HA, NA and M1 mutations increased yield in all three hosts whereas in combination the PB1 and PB2 mutations were host restrictive changing the virus to a mouse specific strain. For the NA and M1 mutations the increase in growth in mouse lung was proportional to a 2-fold (log10) increase in virulence however the HA mutation increased virulence largely independent of increased growth indicating a change in pathological properties that damage the host. Thus mutations that affect virulence can be classified according to host-dependent and independent ability to increase growth as well as changes in pathological properties. Each of the PB1, PB2, NA, HA, and M1 genes acquired gain-of-function mutations for mouse infection that involve structural motifs that may serve as markers for virulence or targets for antiviral therapy.
journal_name
Virus Resjournal_title
Virus researchauthors
Brown EG,Bailly JEdoi
10.1016/s0168-1702(99)00027-1subject
Has Abstractpub_date
1999-05-01 00:00:00pages
63-76issue
1eissn
0168-1702issn
1872-7492pii
S0168-1702(99)00027-1journal_volume
61pub_type
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