Visna virus

Visna virus
Visna virus
Virus classification
Group: Group VI (ssRNA-RT)
Family: Retroviridae
Subfamily: Orthoretrovirinae
Genus: Lentivirus

Visna virus (also known as Visna-Maedi virus, Maedi-Visna virus and ovine lentivirus[1]) from the genus lentivirinae and subfamily Orthoretrovirinae, is a "prototype"[2] retrovirus[3] that causes encephalitis and chronic pneumonitis in sheep.[4] It is known as visna when found in the brain, and maedi when infecting the lungs. Life-long, persistent infections in sheep occur in the lungs, lymph nodes, spleen, joints, central nervous system, and mammary glands;[2][5] The condition is sometimes known as "ovine progressive pneumonia", particularly in the United States,[1] or "Montana Sheep Disease".[6] White blood cells of the monocyte/macrophage lineage are the main target of Visna virus.[7]

Contents

Viral infection

First described in 1954 by Bjorn Sigurdsson in Iceland,[6] Maedi-Visna virus was the first lentivirus to be isolated and characterized, accomplished in 1957 by Sigurdsson.[6][7][8] "Maedi", Icelandic for dyspnoea, and "visna", Icelandic for "wasting"[9] or "shrinking" of the spinal cord, refer to endemic sheep herd conditions that were only found to be related after Sigurdsson's work.[6]

Visna infection may progress to total paralysis leading to death via inanition; however, if helped to obtain water and food, animals may survive for long periods of time, sometimes greater than ten years.[9] Viral replication is almost exclusively associated with macrophages in infected tissues, however replication is restricted in these cells—that is, the majority of cells containing viral RNA do not produce infectious virus.[5]

The disease was introduced to Iceland following an import of Karakul sheep from Germany in 1933.[6] The susceptibility of Maedi-Visna infection varies across sheep breeds, with coarse-wool breeds apparently more susceptible than fine-wool sheep.[6] Attempts at vaccination against Maedi-Visna virus failed to induce immunity, occasionally causing increased viremia and more severe disease.[7] Eradication programs have been established in countries worldwide.[6]

Model system for HIV infection

Though it does not produce severe immunodeficiency, Visna shares many characteristics with human immunodeficiency virus, including the establishment of persistent infection with chronic active lymphoproliferation;[2] however, Visna virus does not infect T-lymphocytes.[7] The relationship of Visna and HIV as lentiviruses was first published in 1985 by Visna researcher Janice E. Clements and colleagues in the HIV field.[10] It has been postulated that the effects of Maedi-Visna infection in sheep are the "equivalent" of central nervous system disease and wasting syndrome found in human AIDS patients.[1][11] Despite limited sequence homology with HIV,[1] the genomic organization of Visna is very similar, allowing Visna infection to be used as an in vivo[12] and in vitro model system for HIV infection.[13][14][15]

Research using Visna was important in the identification and characterization of HIV. Nucleotide sequence analysis demonstrated that the AIDS virus was a retrovirus related to Visna and provided early clues as to the mechanism of HIV infection.[9]

Visna has also been a target for HIV denial hypotheses and conspiracy theories. One such conspiracy theory, promoted by Jakob Segal among others, purports that HIV is a man-made hybrid of Human T-lymphotropic virus maedi-visna.[16]

Control programmes

The maedi-visna control programme of the Swedish Board of Agriculture

Many countries have some sort of national programme to prevent and control a situation where the virus spreads.

References

  1. ^ a b c d Thormar H (2005). "Maedi-visna virus and its relationship to human immunodeficiency virus". AIDS Rev 7 (4): 233–45. PMID 16425963. 
  2. ^ a b c Ryan S, Tiley L, McConnell I, Blacklaws B (November 2000). "Infection of dendritic cells by the Maedi-Visna lentivirus". J. Virol. 74 (21): 10096–103. doi:10.1128/JVI.74.21.10096-10103.2000. PMC 102048. PMID 11024138. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=11024138. 
  3. ^ Wu C, Barbezange C, McConnell I, Blacklaws BA (October 2008). "Mapping and characterization of visna/maedi virus cytotoxic T-lymphocyte epitopes". J. Gen. Virol. 89 (Pt 10): 2586–96. doi:10.1099/vir.0.2008/002634-0. PMID 18796728. http://vir.sgmjournals.org/cgi/pmidlookup?view=long&pmid=18796728. 
  4. ^ Benavides J, García-Pariente C, Fuertes M, et al. (January 2009). "Maedi-visna: the meningoencephalitis in naturally occurring cases". J. Comp. Pathol. 140 (1): 1–11. doi:10.1016/j.jcpa.2008.07.010. PMID 18922546. http://linkinghub.elsevier.com/retrieve/pii/S0021-9975(08)00103-5. 
  5. ^ a b Davis JL, Molineaux S, Clements JE (May 1987). "Visna virus exhibits a complex transcriptional pattern: one aspect of gene expression shared with the acquired immunodeficiency syndrome retrovirus". J. Virol. 61 (5): 1325–31. PMC 254106. PMID 3033262. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=3033262. 
  6. ^ a b c d e f g Straub OC (January 2004). "Maedi-Visna virus infection in sheep. History and present knowledge". Comp. Immunol. Microbiol. Infect. Dis. 27 (1): 1–5. doi:10.1016/S0147-9571(02)00078-4. PMID 14656537. http://linkinghub.elsevier.com/retrieve/pii/S0147-9571(02)00078-4. 
  7. ^ a b c d Torsteinsdottir S, Andresdottir V, Arnarson H, Petursson G (2007). "Immune response to maedi-visna virus". Front. Biosci. 12: 1532–43. doi:10.2741/2166. PMID 17127400. 
  8. ^ SIGURDSSON B, PALSSON P, GRIMSSON H (July 1957). "Visna, a demyelinating transmissible disease of sheep". J. Neuropathol. Exp. Neurol. 16 (3): 389–403. PMID 13439402. 
    SIGURDSSON B, PALSSON PA (October 1958). "Visna of sheep; a slow, demyelinating infection". Br J Exp Pathol 39 (5): 519–28. PMID 13584702. 
  9. ^ a b c Sonigo P, Alizon M, Staskus K, et al. (August 1985). "Nucleotide sequence of the visna lentivirus: relationship to the AIDS virus". Cell 42 (1): 369–82. doi:10.1016/S0092-8674(85)80132-X. PMID 2410140. http://linkinghub.elsevier.com/retrieve/pii/S0092-8674(85)80132-X. 
  10. ^ Gonda MA, Wong-Staal F, Gallo RC, Clements JE, Narayan O, Gilden RV. Sequence homology and morphologic similarity of HTLV-III and visna virus, a pathogenic lentivirus. Science. 1985 Jan 11;227(4683):173-7.
  11. ^ Forsman A, Weiss RA (December 2008). "Why is HIV a pathogen?". Trends Microbiol. 16 (12): 555–60. doi:10.1016/j.tim.2008.09.004. PMID 18977141. http://linkinghub.elsevier.com/retrieve/pii/S0966-842X(08)00227-8. 
  12. ^ Adv Pharmacol. 2000;49:315-85. "HIV-1-associated central nervous system dysfunction." Krebs FC, Ross H, McAllister J, Wigdahl B.
  13. ^ Frank KB, McKernan PA, Smith RA, Smee DF (September 1987). "Visna virus as an in vitro model for human immunodeficiency virus and inhibition by ribavirin, phosphonoformate, and 2',3'-dideoxynucleosides". Antimicrob. Agents Chemother. 31 (9): 1369–74. PMC 174944. PMID 2445282. http://aac.asm.org/cgi/pmidlookup?view=long&pmid=2445282. 
  14. ^ Salvatori D, Vincenzetti S, Maury G, Gosselin G, Gaubert G, Vita A (April 2001). "Maedi-visna virus, a model for in vitro testing of potential anti-HIV drugs". Comp. Immunol. Microbiol. Infect. Dis. 24 (2): 113–22. doi:10.1016/S0147-9571(00)00021-7. PMID 11247044. http://linkinghub.elsevier.com/retrieve/pii/S0147-9571(00)00021-7. 
  15. ^ Salvatori D, Volpini R, Vincenzetti S, et al. (September 2002). "Adenine and deazaadenine nucleoside and deoxynucleoside analogues: inhibition of viral replication of sheep MVV (in vitro model for HIV) and bovine BHV-1". Bioorg. Med. Chem. 10 (9): 2973–80. doi:10.1016/S0968-0896(02)00131-1. PMID 12110319. http://linkinghub.elsevier.com/retrieve/pii/S0968089602001311. 
  16. ^ "Of Myths and Mischief", Discover, 1 December 1994

External links

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