Prevalence of anti-Vif antibodies in HIV-1 infected individuals assessed using recombinant baculovirus expressedVif protein

O’Neil, Caroline A.; Lee, D.; Clewley, G; Ma, Jun; Emery, Vincent C.

doi:10.1002/(sici)1096-9071(199703)51:3<139::aid-jmv1>3.0.co;2-7

Cited by 6 publications

(4 citation statements)

References 28 publications

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“…In our study, anti-ASP antibodies were detected in 10-15% of the HIV-1-infected individuals, which seems less than previously suggested by the study of C. Vaquero, a least for patients in advanced stages of infection (Vanhée-Brossollet et al, 1995). However, humoral responses to other auxiliary and regulatory proteins of HIV-1 in infected subjects ranged from 12% (Tat; Rezza et al, 2005) to 25-26% (Vif and Vpr; Reiss et al, 1990;O'Neil et al, 1997), and up to 43% (Vpu; Reiss et al, 1990). The frequency of anti-ASP antibody response is also consistent with previous studies showing humoral responses against HBZ in 10% of the HTLV-1 infected subjects (Enose-Akahata et al, 2013;Shiohama et al, 2016).…”

Section: Discussioncontrasting

confidence: 71%

A Pilot Study of the Humoral Response Against the AntiSense Protein (ASP) in HIV-1-Infected Patients

et al. 2020

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The existence of an antisense Open Reading Frame (ORF) that encodes a putative AntiSense Protein (ASP) on the proviral genome of Human Immunodeficiency Virus type 1 (HIV-1) was a source of debate for 30 years. During the last years, some progresses have been made to characterize the cellular immune response against ASP in HIV-1 seropositive patients. However, no tools were available for the detection of antibodies to ASP in the plasma of HIV-1-infected patients during the natural course of the infection. The aim of our study was to develop a Luciferase Immuno-Precipitation System (LIPS) to monitor the quantitative detection of ASP-specific antibodies in the plasma of HIV-1-infected patients [antiretroviral therapy (ART) naive-patients, patients under ART and HIV-1 controllers], patients who discontinued antiretroviral drugs (ARV). We further used this approach to delineate the epitopes of ASP targeted by antibodies. Antibodies directed against ASP were detected in 3 out of 19 patients who discontinued ARV (15%) and in 1 out of 10 ART-naive patients (10%), but were neither detected in HIV-1 infected patients under ART nor in HIV-1 controllers. Individual variations in levels of ASP-specific antibodies were detected overtime. Both the conserved prolin-rich motif and the core 60-189 region of ASP were found to be essential for antibody recognition in the four patients tested positive for anti-ASP antibodies, who were all untreated at the time of sampling. Moreover, for two of these patients, increased levels of ASP-specific antibodies were observed concomitantly to viremia declines. Overall, our method may represent a useful tool to detect a humoral response to ASP in HIV-1-infected patients, which allowed us to confirm the expression of ASP during the course of HIV-1 infection. Further studies will be needed to fully characterize the humoral response to ASP in HIV-1-infected patients.

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Section: Discussioncontrasting

confidence: 71%

A Pilot Study of the Humoral Response Against the AntiSense Protein (ASP) in HIV-1-Infected Patients

et al. 2020

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“…In support of the hypothesis that Bet and Vif are differentially expressed in vivo, Bet sero-reactivity is high and has diagnostic value in infected cats and bovines [ 55 , 56 ]. In contrast, while anti-Vif antibodies have been described in HIV patients [ 57 , 58 ], Vif has not been shown to be a major humoral immune target of FIV infection, and seroconversion against Vif has not been well studied in FIV infection (personal communication, Dr. Chris Grant).…”

Section: Discussionmentioning

confidence: 99%

Replacement of feline foamy virus bet by feline immunodeficiency virus vif yields replicative virus with novel vaccine candidate potential

et al. 2018

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BackgroundHosts are able to restrict viral replication to contain virus spread before adaptive immunity is fully initiated. Many viruses have acquired genes directly counteracting intrinsic restriction mechanisms. This phenomenon has led to a co-evolutionary signature for both the virus and host which often provides a barrier against interspecies transmission events. Through different mechanisms of action, but with similar consequences, spumaviral feline foamy virus (FFV) Bet and lentiviral feline immunodeficiency virus (FIV) Vif counteract feline APOBEC3 (feA3) restriction factors that lead to hypermutation and degradation of retroviral DNA genomes. Here we examine the capacity of vif to substitute for bet function in a chimeric FFV to assess the transferability of anti-feA3 factors to allow viral replication.ResultsWe show that vif can replace bet to yield replication-competent chimeric foamy viruses. An in vitro selection screen revealed that an engineered Bet-Vif fusion protein yields suboptimal protection against feA3. After multiple passages through feA3-expressing cells, however, variants with optimized replication competence emerged. In these variants, Vif was expressed independently from an N-terminal Bet moiety and was stably maintained. Experimental infection of immunocompetent domestic cats with one of the functional chimeras resulted in seroconversion against the FFV backbone and the heterologous FIV Vif protein, but virus could not be detected unambiguously by PCR. Inoculation with chimeric virus followed by wild-type FFV revealed that repeated administration of FVs allowed superinfections with enhanced antiviral antibody production and detection of low level viral genomes, indicating that chimeric virus did not induce protective immunity against wild-type FFV.ConclusionsUnrelated viral antagonists of feA3 cellular restriction factors can be exchanged in FFV, resulting in replication competence in vitro that was attenuated in vivo. Bet therefore may have additional functions other than A3 antagonism that are essential for successful in vivo replication. Immune reactivity was mounted against the heterologous Vif protein. We conclude that Vif-expressing FV vaccine vectors may be an attractive tool to prevent or modulate lentivirus infections with the potential option to induce immunity against additional lentivirus antigens.Electronic supplementary materialThe online version of this article (10.1186/s12977-018-0419-0) contains supplementary material, which is available to authorized users.

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“…The abovementioned studies brought strong evidence in favor of the expression of ASP during the course of HIV-1 infection in vivo and strongly suggest that ASP elicits an adaptive response in at least some of the HIV-1-infected patients, as previously described for the other auxiliary and regulatory proteins of HIV-1 that elicit both antibodies and CD8 + T cell responses (Allan et al, 1985;Arya and Gallo, 1986;Kan et al, 1986;Wong-Staal et al, 1987;Chanda et al, 1988;Strebel et al, 1988;Reiss et al, 1990;O'Neil et al, 1997;Rezza et al, 2005;Kiepiela et al, 2007;Cardinaud et al, 2009;Nicoli et al, 2016). Even though the presence of ASP at the surface of infected cells and viral particles was only reported in vitro (Briquet and Vaquero, 2002;Clerc et al, 2011;Laverdure et al, 2012;Affram et al, 2019), it is worth to highlight that an antibody response targeting ASP at the surface of viral particles and infected cells would potentially have interesting implications for the progression of the disease.…”

Section: Asp and Immune Responsementioning

confidence: 72%

“…C-Score = −4.07, estimated TMscore = 0.28 ± 0.09, estimated RMSD = 15.0 ± 3.5 Å. Shiohama et al, 2016) and the auxiliary and regulatory proteins of HIV-1 (Reiss et al, 1990;O'Neil et al, 1997;Rezza et al, 2005). The ASP-specific antibody response was sustained for at least 9 months and seemed to target both the 26-62 residues of ASP bearing the highly conserved proline-rich motif and the core residues 62-141 of ASP (Figures 2, 6A; Savoret et al, 2020).…”

Section: Asp and Immune Responsementioning

confidence: 98%

Antisense Transcripts and Antisense Protein: A New Perspective on Human Immunodeficiency Virus Type 1

et al. 2021

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It was first predicted in 1988 that there may be an Open Reading Frame (ORF) on the negative strand of the Human Immunodeficiency Virus type 1 (HIV-1) genome that could encode a protein named AntiSense Protein (ASP). In spite of some controversy, reports began to emerge some years later describing the detection of HIV-1 antisense transcripts, the presence of ASP in transfected and infected cells, and the existence of an immune response targeting ASP. Recently, it was established that the asp gene is exclusively conserved within the pandemic group M of HIV-1. In this review, we summarize the latest findings on HIV-1 antisense transcripts and ASP, and we discuss their potential functions in HIV-1 infection together with the role played by antisense transcripts and ASPs in some other viruses. Finally, we suggest pathways raised by the study of antisense transcripts and ASPs that may warrant exploration in the future.

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Prevalence of anti-Vif antibodies in HIV-1 infected individuals assessed using recombinant baculovirus expressedVif protein

Cited by 6 publications

References 28 publications

A Pilot Study of the Humoral Response Against the AntiSense Protein (ASP) in HIV-1-Infected Patients

A Pilot Study of the Humoral Response Against the AntiSense Protein (ASP) in HIV-1-Infected Patients

Replacement of feline foamy virus bet by feline immunodeficiency virus vif yields replicative virus with novel vaccine candidate potential

Antisense Transcripts and Antisense Protein: A New Perspective on Human Immunodeficiency Virus Type 1

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