Wild-type equine infectious anemia virus replicates in vivo predominantly in tissue macrophages, not in peripheral blood monocytes
- PMID: 1382143
- PMCID: PMC241467
- DOI: 10.1128/JVI.66.10.5906-5913.1992
Wild-type equine infectious anemia virus replicates in vivo predominantly in tissue macrophages, not in peripheral blood monocytes
Abstract
In situ hybridization of tissues from two horses infected with the wild-type Wyoming strain of equine infectious anemia virus (EIAV) identified the liver, spleen, lymph nodes, kidney, lung, and adrenal gland as the primary host tissue sites for viral transcription during acute infection. Combined immunohistochemistry, with a monoclonal antibody recognizing a cytoplasmic antigen of equine mononuclear phagocytes, and in situ hybridization for viral RNA identified most infected cells as mature tissue macrophages. In contrast, in situ hybridization of adherent peripheral blood mononuclear cells collected from horses on various days during the first 2 weeks postinfection with the Wyoming strain of EIAV failed to detect any viral RNA in these cells. For the two horses described here, serum reverse transcriptase activity correlated directly with the degree of replication detected in tissue macrophages on the day of sacrifice. These results suggest that unlike other lentivirus infections in which mature tissue macrophages accumulate cytoplasmic viral RNA to a high level but fail to produce infectious virions, mature tissue macrophages are the likely primary source of the high titer of viremia present during acute infection with EIAV. No significant posttranscriptional block of viral replication in tissue macrophages appears to occur with EIAV.
Similar articles
-
Monocyte maturation controls expression of equine infectious anemia virus.J Virol. 1994 Oct;68(10):6270-9. doi: 10.1128/JVI.68.10.6270-6279.1994. J Virol. 1994. PMID: 8083967 Free PMC article.
-
Tissue sites of persistent infection and active replication of equine infectious anemia virus during acute disease and asymptomatic infection in experimentally infected equids.J Virol. 2000 Apr;74(7):3112-21. doi: 10.1128/jvi.74.7.3112-3121.2000. J Virol. 2000. PMID: 10708426 Free PMC article.
-
Equine infectious anemia virus replication is upregulated during differentiation of blood monocytes from acutely infected horses.J Virol. 1996 Jan;70(1):590-4. doi: 10.1128/JVI.70.1.590-594.1996. J Virol. 1996. PMID: 8523576 Free PMC article.
-
Immunopathogenesis of equine infectious anemia lentivirus disease.Dev Biol Stand. 1990;72:31-7. Dev Biol Stand. 1990. PMID: 2178127 Review.
-
Regulation of equine infectious anemia virus expression.J Biomed Sci. 1998;5(1):11-23. doi: 10.1007/BF02253351. J Biomed Sci. 1998. PMID: 9570509 Review.
Cited by
-
Equine infectious anemia virus entry occurs through clathrin-mediated endocytosis.J Virol. 2008 Feb;82(4):1628-37. doi: 10.1128/JVI.01754-07. Epub 2007 Dec 5. J Virol. 2008. PMID: 18057237 Free PMC article.
-
The PU.1/Spi-1 proto-oncogene is a transcriptional regulator of a lentivirus promoter.J Virol. 1993 Jul;67(7):3885-90. doi: 10.1128/JVI.67.7.3885-3890.1993. J Virol. 1993. PMID: 8389910 Free PMC article.
-
Infection with equine infectious anemia virus vaccine strain EIAVDLV121 causes no visible histopathological lesions in target organs in association with restricted viral replication and unique cytokine response.Vet Immunol Immunopathol. 2016 Feb;170:30-40. doi: 10.1016/j.vetimm.2016.01.006. Epub 2016 Jan 23. Vet Immunol Immunopathol. 2016. PMID: 26832985 Free PMC article.
-
Interplay of ancestral non-primate lentiviruses with the virus-restricting SAMHD1 proteins of their hosts.J Biol Chem. 2018 Oct 19;293(42):16402-16412. doi: 10.1074/jbc.RA118.004567. Epub 2018 Sep 4. J Biol Chem. 2018. PMID: 30181218 Free PMC article.
-
Human immunodeficiency virus bearing a disrupted central DNA flap is pathogenic in vivo.J Virol. 2007 Jun;81(11):6146-50. doi: 10.1128/JVI.00203-07. Epub 2007 Mar 28. J Virol. 2007. PMID: 17392373 Free PMC article. Review.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources