Human CRM1 Augments Production of Infectious Human and Feline Immunodeficiency Viruses from Murine Cells

Feline immunodeficiency virus
DOI: 10.1128/jvi.01970-12 Publication Date: 2012-08-30T06:03:38Z
ABSTRACT
Productive replication of human immunodeficiency virus type 1 (HIV-1) occurs efficiently only in humans. The posttranscriptional stages the HIV-1 life cycle proceed poorly mouse cells, with a resulting defect viral assembly and release. Previous work has shown that presence chromosome 2 increases production cells. Recent studies have region maintenance (hCRM1) stimulates Gag release from rodent Here we report expressions hCRM1 murine cells resulted marked infectious feline (FIV). was also increased by hSRp40, combination hSRp40 more-than-additive effect on In contrast, overexpression CRM1 (mCRM1) minimally affected FIV did not antagonize hCRM1. there were large amounts released capsid, which paralleled titers. Consistent this finding, ratios unspliced to spliced mRNAs expressing SRp40 became similar those Furthermore, imaging intron-containing RNA showed export cytoplasm.By testing chimeras between mCRM1 comparing sequences CRM1, mapped functional domain HEAT (Huntingtin, elongation factor 3, protein phosphatase 2A, yeast kinase TOR1) repeats 4A 9A triple point mutant repeat 9A, loss function. Structural analysis suggested may serve as binding site for or cellular factors facilitate lentiviral nuclear export.
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