Sequence relationships of type D retroviruses which cause simian acquired immunodeficiency syndrome

Richard M. Thayer, Michael D. Power, Martin L. Bryant, Murray B. Gardner, Philip J. Barr, Paul A Luciw

Research output: Contribution to journalArticle

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Abstract

Simian acquired immunodeficiency syndrome (SAIDS) in macaque monkeys is caused by type D retroviruses; three independent virus isolates are identified as SRV-1 (SAIDS retrovirus-serotype 1), SRV-2, and MPMV (Mason-Pfizer monkey virus). Virions from these three isolates have serologically related core antigens, but distinct surface proteins. Also, SRV-2 is unique since it apparently induces retroperitoneal fibromatosis in addition to SAIDS. The complete DNA sequence of molecularly cloned SRV-2 is presented and compared to the sequences of SRV-1 and MPMV and to the sewuences of other retroviruses and retroviral-related elements in the genomes of eucaryotic cells. SRV-1 and MPMV show fewer than 6% differences in predicted amino acid sequences encoding gag, prt, pol, and the C-terminal env domain; SRV-2 displays about 15-18% differences in these regions when aligned with SRV-1 or MPMV. Greater variation of predicted amino acid sequences is noted in the externally located N-terminal env domains; SRV-1 and MPMV have 83% homology whereas SRV-2 has 58% homology with either SRV-1 or MPMV. Nucleotide sequences of the LTRs of SRV-1 and MPMV are 88% homologous; SRV-2 shows 70% homology with the LTRs of SRV-1 and MPMV. Comparisons of the predicted pol region amino acid sequences of these simian type D retroviruses with the pol gene of a type B retrovirus, mouse mammary tumor virus (MMTV), reveal about 50% homology. A human endogenous element related to the pol region of MMTV shows about 25% homology of amino acids with the pol sequences of SRV-1 or SRV-2. The prt genes of the simian type D retroviruses are similar in size and predicted amino acid sequence with the prt genes of MMTV and the hamster intracisternal type A particle genome. The C-terminal env domains of the avian type C retrovirus reticuloendotheliosis virus (REV) and the type C baboon endogenous virus (BaEV) have 60 and 85% predicted amino acid homology, respectively, with the C-terminal env domains of SRV-1, SRV-2, and MPMV. Within the gag and pol genes of the simian type D retroviruses there are striking homologies with the rat IgE-binding protein gene. Sequence relatedness of these type D retroviruses with type A, type B, and type C retrovirus genomes and with cellular sequences supports the notion that recombinational events contribute to the genesis and variation of retroviruses. These DNA sequence analyses also provide a basis for considering and comparing mechanisms of immunedysfunction mediated by the simian type D retroviruses and other retroviruses..

Original languageEnglish (US)
Pages (from-to)317-329
Number of pages13
JournalVirology
Volume157
Issue number2
DOIs
StatePublished - 1987

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Simian Acquired Immunodeficiency Syndrome
Mason-Pfizer monkey virus
Betaretrovirus
Retroviridae
Simian Retroviruses
Mouse mammary tumor virus
Amino Acid Sequence
pol Genes
Genome
Reticuloendotheliosis virus
Alpharetrovirus
Serogroup

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this

Sequence relationships of type D retroviruses which cause simian acquired immunodeficiency syndrome. / Thayer, Richard M.; Power, Michael D.; Bryant, Martin L.; Gardner, Murray B.; Barr, Philip J.; Luciw, Paul A.

In: Virology, Vol. 157, No. 2, 1987, p. 317-329.

Research output: Contribution to journalArticle

Thayer, Richard M. ; Power, Michael D. ; Bryant, Martin L. ; Gardner, Murray B. ; Barr, Philip J. ; Luciw, Paul A. / Sequence relationships of type D retroviruses which cause simian acquired immunodeficiency syndrome. In: Virology. 1987 ; Vol. 157, No. 2. pp. 317-329.
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N2 - Simian acquired immunodeficiency syndrome (SAIDS) in macaque monkeys is caused by type D retroviruses; three independent virus isolates are identified as SRV-1 (SAIDS retrovirus-serotype 1), SRV-2, and MPMV (Mason-Pfizer monkey virus). Virions from these three isolates have serologically related core antigens, but distinct surface proteins. Also, SRV-2 is unique since it apparently induces retroperitoneal fibromatosis in addition to SAIDS. The complete DNA sequence of molecularly cloned SRV-2 is presented and compared to the sequences of SRV-1 and MPMV and to the sewuences of other retroviruses and retroviral-related elements in the genomes of eucaryotic cells. SRV-1 and MPMV show fewer than 6% differences in predicted amino acid sequences encoding gag, prt, pol, and the C-terminal env domain; SRV-2 displays about 15-18% differences in these regions when aligned with SRV-1 or MPMV. Greater variation of predicted amino acid sequences is noted in the externally located N-terminal env domains; SRV-1 and MPMV have 83% homology whereas SRV-2 has 58% homology with either SRV-1 or MPMV. Nucleotide sequences of the LTRs of SRV-1 and MPMV are 88% homologous; SRV-2 shows 70% homology with the LTRs of SRV-1 and MPMV. Comparisons of the predicted pol region amino acid sequences of these simian type D retroviruses with the pol gene of a type B retrovirus, mouse mammary tumor virus (MMTV), reveal about 50% homology. A human endogenous element related to the pol region of MMTV shows about 25% homology of amino acids with the pol sequences of SRV-1 or SRV-2. The prt genes of the simian type D retroviruses are similar in size and predicted amino acid sequence with the prt genes of MMTV and the hamster intracisternal type A particle genome. The C-terminal env domains of the avian type C retrovirus reticuloendotheliosis virus (REV) and the type C baboon endogenous virus (BaEV) have 60 and 85% predicted amino acid homology, respectively, with the C-terminal env domains of SRV-1, SRV-2, and MPMV. Within the gag and pol genes of the simian type D retroviruses there are striking homologies with the rat IgE-binding protein gene. Sequence relatedness of these type D retroviruses with type A, type B, and type C retrovirus genomes and with cellular sequences supports the notion that recombinational events contribute to the genesis and variation of retroviruses. These DNA sequence analyses also provide a basis for considering and comparing mechanisms of immunedysfunction mediated by the simian type D retroviruses and other retroviruses..

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