Isolation and characterization of a highly divergent HIV-2[GH-2]: Generation of an infectious molecular clone and functional analysis of its rev-responsive element in response to primate retrovirus transactivators (rev and rex)
Identifieur interne : 000014 ( Istex/Corpus ); précédent : 000013; suivant : 000015Isolation and characterization of a highly divergent HIV-2[GH-2]: Generation of an infectious molecular clone and functional analysis of its rev-responsive element in response to primate retrovirus transactivators (rev and rex)
Auteurs : Meiko Kawamura ; Jun Katahira ; Masashi Fukasawa ; Jun-Ichi Sakuragi ; Koh-Ichi Ishikawa ; Masuyo Nakai ; Julius A. A. Mingle ; Mubarak Osei-Kwasi ; Victor B. A. Netty ; Hirofumi Akari ; Osamu Hishida ; Keizo Tomonaga ; Tomoyuki Miura ; Masanori HayamiSource :
- Virology [ 0042-6822 ] ; 1992.
English descriptors
- KwdEn :
- Teeft :
Abstract
A highly divergent HIV-2 designated as HIV-2[GH-2] was obtained from an AIDS-related complex (ARC) patient in Ghana. A full-length molecular clone of this isolate was obtained and a biologically active clone was constructed. Its restriction pattern differed from that of prototype HIV-2[GH-1 ] in 25 of 35 restriction sites, but was strikingly similarto a previously characterized HIV-2 isolate from a Ghanaian (HIV-2ALT). The conserved integrase region (288-bp fragment) previously displayed 95% identity with that of ALT but 17–20% divergence from the HIV-2 prototype member, and a new distinct subgroup (HIV-2b) of HIV-2 consisting of GH-2 and ALT was postulated (Miura et al. 1991.) These isolates, however, were biologically distinguishable from each other by its replication capacity in a monocyte line, U937, in which GH-2 could not grow but ALT grew well. In addition, the nucleotide sequence of the LTR of this new isolate displays 21% divergence from that of prototype HIV-2[GH-1], but the core enhancer, Spl binding sites and TATA box were conserved. Although the 3' half of the env gene sequence which is deleted in HIV-2ALT clone showed 27% diversity from the prototype, functional differences in the rev-responsive element were not observed.
Url:
DOI: 10.1016/0042-6822(92)90540-6
Links to Exploration step
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<front><div type="abstract" xml:lang="en">A highly divergent HIV-2 designated as HIV-2[GH-2] was obtained from an AIDS-related complex (ARC) patient in Ghana. A full-length molecular clone of this isolate was obtained and a biologically active clone was constructed. Its restriction pattern differed from that of prototype HIV-2[GH-1 ] in 25 of 35 restriction sites, but was strikingly similarto a previously characterized HIV-2 isolate from a Ghanaian (HIV-2ALT). The conserved integrase region (288-bp fragment) previously displayed 95% identity with that of ALT but 17–20% divergence from the HIV-2 prototype member, and a new distinct subgroup (HIV-2b) of HIV-2 consisting of GH-2 and ALT was postulated (Miura et al. 1991.) These isolates, however, were biologically distinguishable from each other by its replication capacity in a monocyte line, U937, in which GH-2 could not grow but ALT grew well. In addition, the nucleotide sequence of the LTR of this new isolate displays 21% divergence from that of prototype HIV-2[GH-1], but the core enhancer, Spl binding sites and TATA box were conserved. Although the 3' half of the env gene sequence which is deleted in HIV-2ALT clone showed 27% diversity from the prototype, functional differences in the rev-responsive element were not observed.</div>
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<author xml:id="author-0002"><persName><forename type="first">Masashi</forename>
<surname>Fukasawa</surname>
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<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
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<author xml:id="author-0003"><persName><forename type="first">Jun-Ichi</forename>
<surname>Sakuragi</surname>
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<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
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<author xml:id="author-0004"><persName><forename type="first">Koh-Ichi</forename>
<surname>Ishikawa</surname>
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<author xml:id="author-0005"><persName><forename type="first">Masuyo</forename>
<surname>Nakai</surname>
</persName>
<affiliation>Osaka Medical College, Takatsuki, Osaka, Japan</affiliation>
</author>
<author xml:id="author-0006"><persName><forename type="first">Julius A.A.</forename>
<surname>Mingle</surname>
</persName>
<affiliation>Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana</affiliation>
</author>
<author xml:id="author-0007"><persName><forename type="first">Mubarak</forename>
<surname>Osei-Kwasi</surname>
</persName>
<affiliation>Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana</affiliation>
</author>
<author xml:id="author-0008"><persName><forename type="first">Victor B.A.</forename>
<surname>Netty</surname>
</persName>
<affiliation>St. Joseph Hospital, Koforidua, Ghana</affiliation>
</author>
<author xml:id="author-0009"><persName><forename type="first">Hirofumi</forename>
<surname>Akari</surname>
</persName>
<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
</author>
<author xml:id="author-0010"><persName><forename type="first">Osamu</forename>
<surname>Hishida</surname>
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<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
</author>
<author xml:id="author-0011"><persName><forename type="first">Keizo</forename>
<surname>Tomonaga</surname>
</persName>
<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
</author>
<author xml:id="author-0012"><persName><forename type="first">Tomoyuki</forename>
<surname>Miura</surname>
</persName>
<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
</author>
<author xml:id="author-0013"><persName><forename type="first">Masanori</forename>
<surname>Hayami</surname>
</persName>
<affiliation>To whom reprint requests should be addressed.</affiliation>
<affiliation>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</affiliation>
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<abstract xml:lang="en"><p>A highly divergent HIV-2 designated as HIV-2[GH-2] was obtained from an AIDS-related complex (ARC) patient in Ghana. A full-length molecular clone of this isolate was obtained and a biologically active clone was constructed. Its restriction pattern differed from that of prototype HIV-2[GH-1 ] in 25 of 35 restriction sites, but was strikingly similarto a previously characterized HIV-2 isolate from a Ghanaian (HIV-2ALT). The conserved integrase region (288-bp fragment) previously displayed 95% identity with that of ALT but 17–20% divergence from the HIV-2 prototype member, and a new distinct subgroup (HIV-2b) of HIV-2 consisting of GH-2 and ALT was postulated (Miura et al. 1991.) These isolates, however, were biologically distinguishable from each other by its replication capacity in a monocyte line, U937, in which GH-2 could not grow but ALT grew well. In addition, the nucleotide sequence of the LTR of this new isolate displays 21% divergence from that of prototype HIV-2[GH-1], but the core enhancer, Spl binding sites and TATA box were conserved. Although the 3' half of the env gene sequence which is deleted in HIV-2ALT clone showed 27% diversity from the prototype, functional differences in the rev-responsive element were not observed.</p>
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<head><ce:dochead><ce:textfn>Short communication</ce:textfn>
</ce:dochead>
<ce:title>Isolation and characterization of a highly divergent HIV-2[GH-2]: Generation of an infectious molecular clone and functional analysis of its rev-responsive element in response to primate retrovirus transactivators (rev and rex)</ce:title>
<ce:author-group><ce:author><ce:given-name>Meiko</ce:given-name>
<ce:surname>Kawamura</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="FN1"><ce:sup>1</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Jun</ce:given-name>
<ce:surname>Katahira</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Masashi</ce:given-name>
<ce:surname>Fukasawa</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Jun-Ichi</ce:given-name>
<ce:surname>Sakuragi</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Koh-Ichi</ce:given-name>
<ce:surname>Ishikawa</ce:surname>
<ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Masuyo</ce:given-name>
<ce:surname>Nakai</ce:surname>
<ce:cross-ref refid="AFF3"><ce:sup>‡</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Julius A.A.</ce:given-name>
<ce:surname>Mingle</ce:surname>
<ce:cross-ref refid="AFF4"><ce:sup>§</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Mubarak</ce:given-name>
<ce:surname>Osei-Kwasi</ce:surname>
<ce:cross-ref refid="AFF4"><ce:sup>§</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Victor B.A.</ce:given-name>
<ce:surname>Netty</ce:surname>
<ce:cross-ref refid="AFF5"><ce:sup>|</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Hirofumi</ce:given-name>
<ce:surname>Akari</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Osamu</ce:given-name>
<ce:surname>Hishida</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Keizo</ce:given-name>
<ce:surname>Tomonaga</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Tomoyuki</ce:given-name>
<ce:surname>Miura</ce:surname>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Masanori</ce:given-name>
<ce:surname>Hayami</ce:surname>
<ce:cross-ref refid="COR1"><ce:sup>2</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:affiliation id="AFF1"><ce:label>∗</ce:label>
<ce:textfn>Research Center for Immunodeficiency Virus, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan</ce:textfn>
</ce:affiliation>
<ce:affiliation id="AFF2"><ce:label>†</ce:label>
<ce:textfn>Institute for Public Health, Yamanashi, Japan</ce:textfn>
</ce:affiliation>
<ce:affiliation id="AFF3"><ce:label>‡</ce:label>
<ce:textfn>Osaka Medical College, Takatsuki, Osaka, Japan</ce:textfn>
</ce:affiliation>
<ce:affiliation id="AFF4"><ce:label>§</ce:label>
<ce:textfn>Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana</ce:textfn>
</ce:affiliation>
<ce:affiliation id="AFF5"><ce:label>|</ce:label>
<ce:textfn>St. Joseph Hospital, Koforidua, Ghana</ce:textfn>
</ce:affiliation>
<ce:correspondence id="COR1"><ce:label>2</ce:label>
<ce:text>To whom reprint requests should be addressed.</ce:text>
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<ce:footnote id="FN1"><ce:label>1</ce:label>
<ce:note-para>Present address: Department of Viral Infection, Institute of Medical Science, University of Tokyo, Tokyo, Japan.</ce:note-para>
</ce:footnote>
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<ce:date-received day="16" month="9" year="1991"></ce:date-received>
<ce:date-accepted day="16" month="3" year="1992"></ce:date-accepted>
<ce:abstract><ce:section-title>Abstract</ce:section-title>
<ce:abstract-sec><ce:simple-para>A highly divergent HIV-2 designated as HIV-2[GH-2] was obtained from an AIDS-related complex (ARC) patient in Ghana. A full-length molecular clone of this isolate was obtained and a biologically active clone was constructed. Its restriction pattern differed from that of prototype HIV-2[GH-1 ] in 25 of 35 restriction sites, but was strikingly similarto a previously characterized HIV-2 isolate from a Ghanaian (HIV-2<ce:inf>ALT</ce:inf>
). The conserved integrase region (288-bp fragment) previously displayed 95% identity with that of ALT but 17–20% divergence from the HIV-2 prototype member, and a new distinct subgroup (HIV-2b) of HIV-2 consisting of GH-2 and ALT was postulated (Miura <ce:italic>et al.</ce:italic>
1991.) These isolates, however, were biologically distinguishable from each other by its replication capacity in a monocyte line, U937, in which GH-2 could not grow but ALT grew well. In addition, the nucleotide sequence of the LTR of this new isolate displays 21% divergence from that of prototype HIV-2[GH-1], but the core enhancer, Spl binding sites and TATA box were conserved. Although the 3' half of the env gene sequence which is deleted in HIV-2<ce:inf>ALT</ce:inf>
clone showed 27% diversity from the prototype, functional differences in the rev-responsive element were not observed.</ce:simple-para>
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<abstract lang="en">A highly divergent HIV-2 designated as HIV-2[GH-2] was obtained from an AIDS-related complex (ARC) patient in Ghana. A full-length molecular clone of this isolate was obtained and a biologically active clone was constructed. Its restriction pattern differed from that of prototype HIV-2[GH-1 ] in 25 of 35 restriction sites, but was strikingly similarto a previously characterized HIV-2 isolate from a Ghanaian (HIV-2ALT). The conserved integrase region (288-bp fragment) previously displayed 95% identity with that of ALT but 17–20% divergence from the HIV-2 prototype member, and a new distinct subgroup (HIV-2b) of HIV-2 consisting of GH-2 and ALT was postulated (Miura et al. 1991.) These isolates, however, were biologically distinguishable from each other by its replication capacity in a monocyte line, U937, in which GH-2 could not grow but ALT grew well. In addition, the nucleotide sequence of the LTR of this new isolate displays 21% divergence from that of prototype HIV-2[GH-1], but the core enhancer, Spl binding sites and TATA box were conserved. Although the 3' half of the env gene sequence which is deleted in HIV-2ALT clone showed 27% diversity from the prototype, functional differences in the rev-responsive element were not observed.</abstract>
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