Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have isolated a nonconditional mutant of PR-RSV-E with unique properties. This virus (SE 21Q1b) is shed from a continuously growing culture of transformed quail cells. 21Q1b virions are unable to transform or replicate in other quail or chicken cells after exogenous infection, despite the fact that the viral particles contain normal envelope glycoproteins, internal structural proteins and RNA-dependent DNA polymerase. The lack of infectivity of 21Q1b virions is a consequence of the failure to package genomic 39S RNA. Instead, these virions contain a mixture of heterogenous-sized polyadenylated cellular RNAs and 4S RNA. Less than 1% of the encapsulated RNA is viral-specific, although in the 21Q1b-producing cells, amounts of 39S, 28S and 21S viral RNAs comparable to those in wild-type virus-infected cells are synthesized and function as mRNAs for the viral proteins. Thus 21Q1b can be considered an RNA packaging mutant. Superinfection of 21Q1b cells with either RAV-1 or PR-A leads to production of about 10% or more of the normal titer of superinfecting virus, but none of the 21Q1b genetic markers are rescued. After superinfection, the 21Q1b cells continue to synthesize 21Q1b particles containing cellular RNAs in the same amounts as before infection. Thus superinfection does not appear to "switch off" the aberrant packaging of cellular RNA, but allows packaging of the superinfecting RNA. One explanation for the phenotype of 21Q1b is that the genome is lacking a signal necessary for efficient genomic RNA packaging (but not for translation) and that the 21Q1b genome encodes a "packaging factor" with an altered specificity so that cellular RNAs are efficiently packaged. 21Q1b virions do contain RNA-dependent DNA polymerase which has normal endogenous synthetic activity. The cDNA product made in vitro from detergent-lysed 21Q1b virions hybridizes equally well to uninfected quail and 21Q1b-producing quail cell RNAs, with kinetics suggesting that the endogenous product consists of transcripts of cellular RNAs present in low amounts in the cells.
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PMID:An avian oncovirus mutant (SE 21Q1b) deficient in genomic RNA: biological and biochemical characterization. 8 99

Superinfection of chicken embryo fibroblasts transformed by the defective Bryan strain of Rous sarcoma virus (BH-RSV) with two different reticuloendotheliosis viruses (REVs), REV strain T (REV-T) or spleen necrosis virus (SNV), resulted in the production of infectious sarcoma virus pseudotypes. These pseudotypes were neutralized by antiserum prepared against SNV and were unable to infect chicken cells preinfected with either REV-T or SNV. These results suggest that defective BH-RSV is able to use the glycoprotein from REV to form infectious pseudotypes. On the other hand, neither REV-T nor SNV was able to supply a functional reverse transcriptase to the polymerase-negative mutant BH-RSValpha, nor was REV-T or SNV able to complement the defect in the internal protein gene of the temperature-sensitive avian sarcoma virus mutant NY45.
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PMID:Formation of reticuloendotheliosis virus pseudotypes of Rous sarcoma virus. 19 82

Cell clones nonproductively transformed by the replication-defective Abelson strain of murine leukemia virus (AbLV) were analyzed for type C viral antigen expression by competition immunoassay. AbLV-transformed mink non-producer lines were found to express a 110,000- to 130,000-molecular weight polyprotein containing murine leukemia virus gag proteins p15 and p12 covalently linked to nonstructural AbLV-coded component(s) of around 80,000-100,000 molecular weight. This polyprotein lacked detectable antigenic cross-reactivity with other virion-coded gag gene proteins such as p30, p10, the viral reverse transcriptase (RNA-dependent DNA polymerase), or the major viral envelope glycoprotein, gp70. By analogy to earlier data on feline and avian sarcoma viruses, these results suggest that a portion of this polyprotein might represent the AbLV src gene product and that in translation it is initially linked in precursor form to gag structural proteins. Superinfection of mink cells nonproductively transformed by AbLV--with either a wild mouse amphotropic type C virus isolate, 4070-A, or with the endogenous cat virus, RD114--led to production of pseudotype virus containing high concentrations of the AbLV-coded precursor polyprotein.
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PMID:Cells nonproductively transformed by Abelson murine leukemia virus express a high molecular weight polyprotein containing structural and nonstructural components. 21 10

In the past, positive as well as negative results pertaining to HIV-1/HIV2 interference have been obtained. Therefore, in the present study attention was paid to the viral expression state of preinfected cells at the time of exposure to secondary virus. A clonal HIV-2 infected HUT-78 cell line was derived by endpoint dilution and subsequently inoculated with cell-free HIV-1. Superinfection with HIV-1 was ruled out by Western blot and PCR analysis. The chronically HIV-2 infected cells used for these studies showed a highly productive expression state, as evidenced by immunoperoxidase staining (IPS), Western blot profile and levels of reverse transcriptase (RT) activity. We discuss several mechanisms of interference in productively infected cells, which may confer resistance to superinfection with secondary virus.
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PMID:Productive expression state confers resistance of human immunodeficiency virus (HIV)-2-infected lymphoma cells against superinfection by HIV-1. 834 81

Superinfection by HIV-1 of a cell line containing the complete murine leukemia virus (MuLV) genome was shown to give rise to pseudotyped HIV-1/MuLV. Such superinfection was successful with certain strains of HIV-1 subtypes A-D. Primary spleen cells and cells of the peritoneal cavity of immunocompetent mice of the C57Bl/6 strain were infectable with the pseudotype HIV-1/MuLV and secreted HIV-1 in vitro and in vivo. In contrast, the murine cell lines, NIH 3T3, myeloma cell line Sp2/0, and two murine hybridoma cell lines were relatively resistant to infection and produced no or little HIV. After primary murine spleen cells had been infected with pseudotyped HIV-1 and transferred to C57Bl/6 mice, replication-competent HIV-1 was obtained from the peritoneal cavity for at least 10-14 days. High amounts (> 10(5) vRNA copies/ml) of HIV-1 vRNA could be measured in the peritoneal fluid. Presence of HIV-1 proviral DNA was detectable in cells from the peritoneal cavity for up to 24 days after infected cell transfer. Active reverse transcriptase representing both HIV-1 and C-type murine retroviruses was detected in the peritoneal washes. The HIV-infected spleen cells injected into the peritoneal cavity elicited HIV-1-specific cellular immune responses to p24gag, gp160Env, Nef, Tat and Rev. Mice immunized with HIV-1 DNA, but not with HIV-1 protein, cleared their HIV-1-infected cells within 10-14 days after challenge with HIV-1/MuLV-infected syngeneic spleen cells. This novel model system of primarily cellular reactivity to HIV-1-infected cells in vivo may become useful for assaying experimental HIV-1 immunization schedules.
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PMID:Genetic immunization with multiple HIV-1 genes provides protection against HIV-1/MuLV pseudovirus challenge in vivo. 1538 91

Human immunodeficiency virus type 2 (HIV-2) was isolated in AIDS patients in 1986. Around 1-2 million people are infected worldwide. The virus is less transmissible than HIV-1, being sexual contacts the most frequent route of acquisition. In the absence of antiretroviral therapy, most HIV-2 carriers will develop AIDS; however, it takes longer than in HIV-1 infection. There is no global pandemic caused by HIV-2, as the virus is largely confined to West Africa. Due to historical ties, HIV-2 is also prevalent in Portugal and its former colonies in Brazil, India, Mozambique, and Angola. Other European countries with hundreds to thousands of HIV-2 infections are France, Belgium, and Spain. A few hundred have been reported in North America, mostly in West African foreigners. Globally, HIV-2 infections are steadily declining. Although CD4 declines occur more slowly in HIV-2 than in HIV-1 patients, the CD4 recovery with antiretroviral treatment is smaller in the former. HIV-2 is naturally resistant to non-nucleoside reverse transcriptase inhibitors (NNRTIs) and some protease inhibitors. In contrast, HIV-2 is susceptible to all NRTIs and integrase inhibitors. Drug resistance in HIV-2 may develop earlier than in HIV-1 and select for mutations at distinct sites. Misdiagnosis of HIV-2 in patients wrongly considered as HIV-1 positive or in those dually infected may result in treatment failures with undetectable HIV-1RNA. Given the relatively large number of West Africans migrated to the European Union and North America, HIV-2 infection either alone or as coinfection with HIV-1 should be excluded at least once in all HIV-seroreactive persons. This should be stressed in the face of atypical HIV serological profiles, immunovirological disconnect (CD4 cell count loss despite undetectable HIV-1 viremia), and/or high epidemiological risks (birth in or sex partners from HIV-2 endemic regions). Superinfection with any HIV variant may occur in persons infected with the other, since there is no cross-protection. Thus, earlier antiretroviral therapy is warranted for either HIV-1 or HIV-2, given that it would protect from each other superinfection in persons at risk.
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PMID:Antiretroviral Therapy for HIV-2 Infection in Non-Endemic Regions. 3216 6