Human Retrovirus Research Articles

50th anniversary of the discovery of reverse transcriptase.

The simultaneous discovery in 1970 of reverse transcriptase in virions of retroviruses by Howard Temin and David Baltimore was perhaps the most dramatic scientific moment of the second half of the 20th century. Ten years previously, Temin’s observation of cells transformed by Rous Sarcoma virus led him to the conclusion that retroviruses replicate through a DNA intermediate he called the provirus. This heretical hypothesis was greeted with derision by fellow scientists; Temin and Baltimore performed a simple experiment, rapidly reproduced, and convincing to all. Its result was a major paradigm shift—reversal of the central dogma of molecular biology. It immediately grabbed the attention of both the scientific and lay press. It also came at a key time for cancer research, at the start of the “War on Cancer.” As a theoretical base and fundamental molecular tool, it enabled a decade of (largely fruitless) search for human oncogenic retroviruses but laid the foundation for the discovery of HIV 13 years later, leading to the development of effective therapy. I had the good fortune, as a student in Temin’s lab, to witness these events. I am honored to be able to share my recollection on the occasion of their 50th anniversary.

Classification of Retroviruses Based on Genomic Data Using RVGC

Retroviruses are a large group of infectious agents with similar virion structures and replication mechanisms. AIDS, cancer, neurologic disorders, and other clinical conditions can all be fatal due to retrovirus infections. Detection of retroviruses by genome sequence is a biological problem that benefits from computational methods. The National Center for Biotechnology Information (NCBI) promotes science and health by making biomedical and genomic data available to the public. This research aims to classify the different types of rotavirus genome sequences available at the NCBI. First, nucleotide pattern occurrences are counted in the given genome sequences at the preprocessing stage. Based on some significant results, the number of features used for classification is reduced to five. The classification shall be carried out in two phases. The first phase of classification shall select only two features. Unclassified data in the first phase is transferred to the next phase, where the final decision is taken with the remaining three features. Three data sets of animals and human retroviruses are selected; the training data set is used to minimize the classifier’s number and training; the validation data set is used to validate the models. The performance of the classifier is analyzed using the test data set. Also, we use decision tree, naive Bayes, k-nearest neighbors, and vector support machines to compare results. The results show that the proposed approach performs better than the existing methods for the retrovirus’s imbalanced genome-sequence dataset.

Hairy Projections on Non Hairy Cells- A Case Report

Adult T-Cell Leukaemia/Lymphoma (ATLL) is a mature T-cell neoplasm. It is caused by human retrovirus Human T-cell Lymphotropic Virus Type 1(HTLV-1). The neoplastic cells after monoclonal integration begin to express T-cell associated antigens namely CD2, CD3 and CD5. These leukaemic cells are highly pleomorphic in light microscopic appearance and also they have a highly variable clinical presentation ranging from acute to lymphomatous to chronic to smouldering. There is a chance of missed or miss diagnosis due to their morphological and clinical heterogeneity and specialised test like immunophenotyping or flow cytometry is essential for exact categorisation. Authors hereby, report a case of 45-year-old female patient suffering from ATLL whose peripheral smear showed leukaemic cells with unusual hairy projections resembling hairy cell leukaemia posing diagnostic dilemma.

CRISPR Genome Editing Applied to the Pathogenic Retrovirus HTLV-1.

CRISPR editing of retroviral proviruses has been limited to HIV-1. We propose human T-cell leukemia virus type 1 (HTLV-1) as an excellent model to advance CRISPR/Cas9 genome editing technologies against actively expressing and latent retroviral proviruses. HTLV-1 is a tumorigenic human retrovirus responsible for the development of both leukemia/lymphoma (ATL) and a neurological disease (HAM/TSP). The virus immortalizes and persists in CD4+ T lymphocytes that survive for the lifetime of the host. The most important drivers of HTLV-1-mediated transformation and proliferation are the tax and hbz viral genes. Tax, transcribed from the plus-sense or genome strand, is essential for de novo infection and cellular immortalization. Hbz, transcribed from the minus-strand, supports proliferation and survival of infected cells in both its protein and mRNA forms. Abrogating the function or expression of tax and/or hbz by genome editing and mutagenic double-strand break repair may disable HTLV-1-infected cell growth/survival and prevent immune modulatory effects and ultimately HTLV-1-associated disease. In addition, the HTLV-1 viral genome is highly conserved with remarkable sequence homogeneity, both within the same host and even among different HTLV isolates. This offers more focused guide RNA targeting. In addition, there are several well-established animal models for studying HTLV-1 infection in vivo as well as cell immortalization in vitro. Therefore, studies with HTLV-1 may provide a better basis to assess and advance in vivo genome editing against retroviral infections.

Beijing as the hub of CRF07_BC transmission from the intravenous drug users to men who have sex with men in China.

The HIV-1 CRF07_BC strain has been increasing in frequency in China, is now the major recombination subtype in the men who have sex with men (MSM) population. However, to date, the evolutionary history of CRF07_BC in MSM in China has not been explored in greater detail. All available partial gag, pol and env segments of CRF07_BC were obtained from the Los Alamos HIV database. We performed phylogenetic analysis for these fragments by using the Bayesian Markov Chain Monte Carlo method, as implemented in BEAST. We estimated the history of viral migration between different areas over time using the discrete Bayesian phylogeographical method. Spatial reconstruction showed that Yunnan had the highest root state posterior probability (0.89 in pol, 0.60 in gag, 0.87 in env). The virus migrated from Yunnan to Beijing in 1990s through intravenous drug users (IDU). The highest root state posterior probability of MSM cluster is Beijing (0.93 in pol, 0.90 in gag and 0.37 in env). In the beginning of 2000s, Beijing became the primary epicenter as CRF07_BC had expanded their geographical distribution to many provinces in China in MSM population. Guangdong and Shanghai were secondary epicenters, with a large extent of viruses. This study highlighted the spatial and temporal spread of CRF07_BC in MSM population in China. It revealed that Beijing was the hub of CRF07_BC transmission from IDU to MSM in China.

Seroprevalence of Hepatitis B and C and Associated Risk Factors among HIV-1 Infected Patients in a High Risk Border Region of South West Cameroon

Coinfection of HIV with human retroviruses such as hepatitis B (HBV) and hepatitis C (HCV) has been associated with adverse liver disease outcomes including reduced survival, cancer and antiretroviral induced hepatotoxicity. In this study, we evaluated the prevalence of hepatitis B surface antigen (HBsAg) and hepatitis C antibody (HCVAb) among HIV-infected individuals diagnosed within six months in South West Cameroon and identified risk factors of coinfection.

An appraisal on quality of life in AIDS patient

Quality of life is the expectation of the individual or society for a good life which outline both positive and negative features of life. Acquired immunodeficiency disease is caused by human retrovirus which was considered as a fat illness before the introduction of proper treatment. Symptoms of the disease include flu like illness, skin rash, sore throat, opportunistic infections, enlarged lymohnodes in necks and so on. According to Who ,since the beginning of pandemic 76 million people have been infected with hiv virus and about 33 million deaths has been reported. At the end of 2019 about 38.0 million people were living with the disease globally. Antiretroviral drugs are used for the treatment of human immune deficiency virus. The review paper was prepared by referring review and research papers from research gate, pubmed, goggle scholar, science direct and search was based on key words such as AIDS, HAART, Quality of life in Aids patients. Aids was considered as a fatal illness till the introduction of proper treatment regimen. The morbidity, mortality and disease severity was reduced to a great extent by antiretroviral drugs. Quality of life was also seen to be improved in patients. Social support has a positive impact on quality of life. Factors like depression, emotional stress, unemployment, suicidal ideation affect the quality of life in AIDS patients.

Retraction of: Association Between Polymorphisms in the Interleukin-10 Gene and Susceptibility to HIV-1 Infection," by Dan-Hui Fu, Wen-Juan Deng, Zhi Yang, Sen Hong, Qian-Ling Ding, Yang Zhao, Jia Chen, and Dan-Ke Su; AIDS Res Hum Retroviruses, epub: 16 Jun 2020; DOI: 10.1089/AID.2020.0011).

AIDS Research and Human RetrovirusesVol. 36, No. 10 RetractionOpen AccessRetraction of: Association Between Polymorphisms in the Interleukin-10 Gene and Susceptibility to HIV-1 Infection,” by Dan-Hui Fu, Wen-Juan Deng, Zhi Yang, Sen Hong, Qian-Ling Ding, Yang Zhao, Jia Chen, and Dan-Ke Su; AIDS Res Hum Retroviruses, epub: 16 Jun 2020; DOI: 10.1089/AID.2020.0011This article retracts the following:Retracted: Association between polymorphisms in the interleukin-10 gene and susceptibility to HIV-1 infectionPublished Online:5 Oct 2020https://doi.org/10.1089/aid.2020.0011.retractAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail AIDS Research and Human Retroviruses officially retracts the paper entitled, “Association Between Polymorphisms in the Interleukin-10 Gene and Susceptibility to HIV-1 Infection,” by Dan-Hui Fu, Wen-Juan Deng, Zhi Yang, Sen Hong, Qian-Ling Ding, Yang Zhao, Jia Chen, and Dan-Ke Su (AIDS Res Hum Retroviruses, epub: 16 Jun 2020; DOI: 10.1089/AID.2020.0011) due to a final, post-acceptance plagiarism review of the paper revealed a level of duplication of published sources that exceeded normal thresholds. The authors were provided an opportunity to adjust the problem, but the revision was returned with an even higher degree of duplication.The Editor and Publisher of AIDS Research and Human Retroviruses are committed to preserving the scientific literature and the community it serves.FiguresReferencesRelatedDetailsRelated articlesRetracted: Association between polymorphisms in the interleukin-10 gene and susceptibility to HIV-1 infection16 Jun 2020AIDS Research and Human Retroviruses Volume 36Issue 10Oct 2020 InformationCopyright 2020, Mary Ann Liebert, Inc., publishersTo cite this article:AIDS Research and Human Retroviruses.Oct 2020.881-881.http://doi.org/10.1089/aid.2020.0011.retractPublished in Volume: 36 Issue 10: October 5, 2020Online Ahead of Print:September 28, 2020PDF download

Identification of Modulators of HIV-1 Proviral Transcription from a Library of FDA-Approved Pharmaceuticals.

Human immunodeficiency virus 1 (HIV-1) is the most prevalent human retrovirus. Recent data show that 34 million people are living with HIV-1 worldwide. HIV-1 infections can lead to AIDS which still causes nearly 20,000 deaths annually in the USA alone. As this retrovirus leads to high morbidity and mortality conditions, more effective therapeutic regimens must be developed to treat these viral infections. A key target for intervention for which there are no current FDA-approved modulators is at the point of proviral transcription. One successful method for identifying novel therapeutics for treating infectious diseases is the repurposing of pharmaceuticals that are approved by the FDA for alternate indications. Major benefits of using FDA-approved drugs include the fact that the compounds have well established toxicity profiles, approved manufacturing processes, and immediate commercial availability to the patients. Here, we demonstrate that pharmaceuticals previously approved for other indications can be utilized to either activate or inhibit HIV-1 proviral transcription. Specifically, we found febuxostat, eltrombopag, and resveratrol to be activators of HIV-1 transcription, while mycophenolate was our lead inhibitor of HIV-1 transcription. Additionally, we observed that the infected cells of lymphoid and myeloid lineage responded differently to our lead transcriptional modulators. Finally, we demonstrated that the use of a multi-dose regimen allowed for enhanced activation with our transcriptional activators.

Flossie Wong-Staal (1946–2020)

Trailblazing HIV researcher

Non-cytotoxic 1,2,3-triazole tethered fused heterocyclic ring derivatives display Tax protein inhibition and impair HTLV-1 infected cells

Human T cell lymphotropic virus type 1 (HTLV-1) is a human retrovirus that infects approximately 10–20 million people worldwide and causes an aggressive neoplasia (adult T-cell leukemia/lymphoma - ATL). Therapeutic approaches for the treatment of ATL have variable effectiveness and poor prognosis, thus requiring strategies to identify novel compounds with activity on infected cells. In this sense, we initially screened a small series of 25 1,2,3-triazole derivatives to discover cell proliferation inhibitors and apoptosis inducers in HTLV-1-infected T-cell line (MT-2) for further assessment of their effect on viral tax activity through inducible-tax reporter cell line (Jurkat LTR-GFP). Eight promising compounds (02, 05, 06, 13, 15, 21, 22 and 25) with activity ≥70% were initially selected, based on a suitable cell-based assay using resazurin reduction method, and evaluated towards cell cycle, apoptosis and Tax/GFP expression analyses through flow cytometry. Compound 02 induced S phase cell cycle arrest and compounds 05, 06, 22 and 25 promoted apoptosis. Remarkably, compounds 22 and 25 also reduced GFP expression in an inducible-tax reporter cell, which suggests an effect on Tax viral protein. More importantly, compounds 02, 22 and 25 were not cytotoxic in human hepatoma cell line (Huh-7). Therefore, the discovery of 3 active and non-cytotoxic compounds against HTLV-1-infected cells can potentially contribute, as an initial promising strategy, to the development process of new drugs against ATL.

The state of latency in microbial pathogenesis.

The state of latency occurs when a microbe's persistence in a host produces host damage without perturbing homeostasis sufficiently to cause clinical symptoms or disease. The mechanisms contributing to latency are diverse and depend on the nature of both the microbe and the host. Latency has advantages for both host and microbe. The host avoids progressive damage caused by interaction with the microbe that may translate into disease, and the microbe secures a stable niche in which to survive. Latency is clinically important because some latent microbes can be transmitted to other hosts, and it is associated with a risk for recrudescent microbial growth and development of disease. In addition, it can predispose the host to other diseases, such as malignancies. Hence, latency is a temporally unstable state with an eventual outcome that mainly depends on host immunity. Latency is an integral part of the pathogenic strategies of microbes that require human (and/or mammalian) hosts, including herpesviruses, retroviruses, Mycobacterium tuberculosis, and Toxoplasma gondii. However, latency is also an outcome of infection with environmental organisms such as Cryptococcus neoformans, which require no host in their replicative cycles. For most microbes that achieve latency, there is a need for a better understanding and more investigation of host and microbial mechanisms that result in this state.

Contribution of Human Retroviruses to Disease Development-A Focus on the HIV- and HERV-Cancer Relationships and Treatment Strategies.

Animal retroviruses are known for their transforming potential, and this is also true for the ones hosted by humans, which have gathered expanding attention as one of the potent causative agents in various disease, including specific cancer types. For instance, Human T Lymphotropic virus (HTLV) is a well-studied class of oncoviruses causing T cell leukemia, while human immunodeficiency virus (HIV) leads to acquired immunodeficiency syndrome (AIDS), which is linked to a series of defining cancers including Kaposi sarcoma, certain types of non-Hodgkin lymphoma, and cervical cancer. Of note, in addition to these “modern” exogenous retroviruses, our genome harbors a staggering number of human endogenous retroviruses (HERVs). HERVs are the genetic remnants of ancient retroviral germline infection of human ancestors and are typically silenced in normal tissues due to inactivating mutations and sequence loss. While some HERV elements have been appropriated and contribute to human physiological functions, others can be reactivated through epigenetic dysregulations to express retroviral elements and promote carcinogenesis. Conversely, HERV replication intermediates or protein products can also serve as intrinsic pathogen-associated molecular patterns that cause the immune system to interpret it as an exogenous infection, thereby stimulating immune responses against tumors. As such, HERVs have also been targeted as a potential internal strategy to sensitize tumor cells for promising immunotherapies. In this review, we discuss the dynamic role of human retroviruses in cancer development, focusing on HIV and HERVs contribution. We also describe potential treatment strategies, including immunotherapeutic targeting of HERVs, inhibiting DNA methylation to expose HERV signatures, and the use of antiretroviral drugs against HIV and HERVs, which can be employed as prospective anti-cancer modalities.

Laboratory Diagnosis of HTLV-1-Associated Myelopathy

Human T-lymphotropic virus type 1 (HTLV-1), a human retrovirus, is endemic in certain regions of the world and affects millions of people worldwide. Infected individuals are at risk of developing adult T-cell leukemia/lymphoma and HTLV-1-associated myelopathy/tropical spastic paraparesis. Vertical and parenteral transmission are the main routes of infection. Diagnosis of HTLV-1 infection can be made by detection of HTLV-1-specific antibodies in plasma, serum, or cerebrospinal fluid using a combination of initial and supplemental serologic assays. In contrast, quantitative proviral DNA in peripheral blood mononuclear cells has been used to predict and monitor disease progression. This review provides an overview of the virology, epidemiology, transmission, pathophysiology, clinical manifestations, and laboratory testing methods for HTLV-1 infection.

Rapid and label-free electrochemical DNA biosensor based on a facile one-step electrochemical synthesis of rGO-PPy-(L-Cys)-AuNPs nanocomposite for the HTLV-1 oligonucleotide detection.

Human T cell leukemia virus type 1 (HTLV-1) as the first human retrovirus is currently a serious endemic health challenge. Despite the use of assorted molecular or serological assays for HTLV-1 detection, there are several limitations due to the lack of a confirmatory test that may affect the accuracy of the results. Herein, a novel label-free biosensor for the detection of HTLV-1 Tax gene has been reported. An electrochemical facile ecofriendly synthesis method has been demonstrated based on a synthesis of nanocomposite of reduced graphene oxide, polypyrrole, and gold nanoparticles (rGO-PPy-(l-Cys)-AuNPs) deposited on the surface of screen-printed carbon electrode. Electrochemical techniques were used to characterize and study the electrochemical behavior of the rGO-PPy-(l-Cys)-AuNPs, which exhibited a stable reference peak at 0.21V associated with hybridization forms by applying the differential pulse voltammetry. The designed DNA biosensor presented a wide linear range from 0.1fM to 100µM and a low detection limit of 20 atto-molar. The proposed biosensor presented in this study provides outstanding selectivity, sensitivity, repeatability, and reproducibility.

HTLV in South America: Origins of a silent ancient human infection.

The description of the first human retrovirus, human T-lymphotropic virus 1 (HTLV-1), was soon associated with an aggressive lymphoma and a chronic inflammatory neurodegenerative disease. Later, other associated clinical manifestations were described, affecting diverse target organs in the human body and showing the enormous burden carried by the virus and the associated diseases. The epidemiology of HTLV-1 and HTLV-2 showed that they were largely distributed around the world, although it is possible to locate geographical areas with pockets of low and very high prevalence and incidence. Aboriginal Australians and indigenous peoples of Brazil are examples of the large spread of HTLV-1 and HTLV-2, respectively. The epidemiological link of both situations is their occurrence among isolated, epidemiologically closed or semi-closed communities. The origin of the viruses in South America shows two different branches with distinct timing of entry. HTLV-1 made its probable entrance in a more recent route through the east coast of Brazil at the beginning of the slave trade from the African continent, starting in the 16th century and lasting for more than 350 years. HTLV-2 followed the ancient route of human migration from the Asian continent, crossing the Behring Strait and then splitting in South America as the population became separated by the Andes Mountains. By that time, HTLV-2c probably arose and became isolated among the indigenous populations in the Brazilian Amazon. The study of epidemiologically closed communities of indigenous populations in Brazil allowed tracing the most likely route of entry, the generation of a new molecular subtype (HTLV-2c), the elucidation of the vertical transmission of HTLV-2, the intrafamilial aggregation of cases and the escape and spread of the virus to other areas in Brazil and abroad. Despite the burden and impact of both viruses, they are maintained as silent infections among human populations because 1, health authorities in most South American countries in which national surveillance is poor have little interest in the disease, 2, the information is commonly lost as indigenous groups do not have specific policies for HTLV and other sexually transmitted infections, and 3, health access is not feasible or properly delivered.

The effect of alcoholic extract from Eucalyptus camaldulensis leaves on HTLV-1 Tax activities

ABSTRACT HTLV-1 is a human retrovirus responsible for adult T-cell leukemia (ATL) and certain other clinical disorders. The viral Tax oncoprotein plays a central role in HTLV-1 pathogenicity, mainly due to its capacity of inducing the transcriptional activity of various transcriptional factors like NFқB. Eucalyptus camaldulensis (Ec) is considered as a traditional medicinal plant with valuable therapeutic effects. Here we evaluated the activity of its ethanolic leave extract on different Tax activities by testing its influence on Tax-induced activity of NFқB and HTLV-1 LTR in Jurkat cells. Our results showed that Ec inhibited Tax induced activation of NFқB -, SRF- dependent promoters and HTLV-1 LTR. Ec extract has no effect on the binding of Tax to NFқB while it strongly prevented the degradation of IҝBα induced by Tax probably as a result of preventing the link between Tax and IKKγ. In addition, increasing the cellular level of P-TEFb-cyclinT1 significantly reduced the inhibitory effect of Ec on Tax activities, probably by preventing the interaction between Tax and P-TEFb-cyclin T1. The 40%-MeOH fraction of this extract, which is rich with polyphenols, offered the highest inhibitory effect against Tax activities. Further studies are required for the isolation and identification of active component/s in this extract which may be developed in the future as preventive/curing drugs for HTLV-1 related diseases.

RETRACTED: Association Between Polymorphisms in the Interleukin-10 Gene and Susceptibility to HIV-1 Infection.

AIDS Research and Human Retroviruses officially retracts the paper entitled, "Association Between Polymorphisms in the Interleukin-10 Gene and Susceptibility to HIV-1 Infection," by Dan-Hui Fu, Wen-Juan Deng, Zhi Yang, Sen Hong, Qian-Ling Ding, Yang Zhao, Jia Chen, and Dan-Ke Su (AIDS Res Hum Retroviruses, epub: 16 Jun 2020; DOI: 10.1089/AID.2020.0011) due to a final, post-acceptance plagiarism review of the paper revealed a level of duplication of published sources that exceeded normal thresholds. The authors were provided an opportunity to adjust the problem, but the revision was returned with an even higher degree of duplication. The Editor and Publisher of AIDS Research and Human Retroviruses are committed to preserving the scientific literature and the community it serves.

Reversal of Epigenetic Silencing Allows Robust HIV-1 Replication in the Absence of Integrase Function.

Integration of the proviral DNA intermediate into the host cell genome normally represents an essential step in the retroviral life cycle. While the reason(s) for this requirement remains unclear, it is known that unintegrated proviral DNA is epigenetically silenced. Here, we demonstrate that human immunodeficiency virus 1 (HIV-1) mutants lacking a functional integrase (IN) can mount a robust, spreading infection in cells expressing the Tax transcription factor encoded by human T-cell leukemia virus 1 (HTLV-1). In these cells, HIV-1 forms episomal DNA circles, analogous to hepatitis B virus (HBV) covalently closed circular DNAs (cccDNAs), that are transcriptionally active and fully capable of supporting viral replication. In the presence of Tax, induced NF-κB proteins are recruited to the long terminal repeat (LTR) promoters present on unintegrated HIV-1 DNA, and this recruitment in turn correlates with the loss of inhibitory epigenetic marks and the acquisition of activating marks on histones bound to viral DNA. Therefore, HIV-1 is capable of replication in the absence of integrase function if the epigenetic silencing of unintegrated viral DNA can be prevented or reversed.IMPORTANCE While retroviral DNA is synthesized normally after infection by integrase-deficient viruses, the resultant episomal DNA is then epigenetically silenced. Here, we show that expression of the Tax transcription factor encoded by a second human retrovirus, HTLV-1, prevents or reverses the epigenetic silencing of unintegrated HIV-1 DNA and instead induces the addition of activating epigenetic marks and the recruitment of NF-κB/Rel proteins to the HIV-1 LTR promoter. Moreover, in the presence of Tax, the HIV-1 DNA circles that form in the absence of integrase function are not only efficiently transcribed but also support a spreading, pathogenic integrase-deficient (IN-) HIV-1 infection. Thus, retroviruses have the potential to replicate without integration, as is indeed seen with HBV. Moreover, these data suggest that integrase inhibitors may be less effective in the treatment of HIV-1 infections in individuals who are also coinfected with HTLV-1.

The reasons to include the serology of human T-lymphotropic virus types 1 and 2 (HTLV-1 and HTLV-2) in the clinical follow-up of patients with viral hepatitis B and C in Brazil.

BackgroundThe WHO established targets for 2030 to globally reduce new viral hepatitis B and C infections by 90% and deaths by 65% and recommends searching for coinfections that increase the progression of chronic liver infections towards cirrhosis and hepatocellular carcinoma.Aims and methodologyThis study aimed to add information concerning the influence of human T-lymphotropic virus type 1 (HTLV-1) and type 2 (HTLV-2) infections in hepatitis B and C, since in Brazil, these human retroviruses are endemic but neglected. Serum samples from 1,910 patients with hepatitis B and 1,315 with hepatitis C from São Paulo, southeast Brazil, that were previously tested and grouped for HIV and HTLV-1/-2 coinfections were analyzed for hepatitis B virus (HBV) and hepatitis C virus (HCV) loads measurements and subsequent clearance using data from laboratory records.Key resultsBriefly, the lowest HBV viral load (VL) was detected in HBV/HTLV-2 coinfected patients, regardless of whether they were infected with HIV (all comparisons p<0.05). In contrast, higher HCV VL was detected in HCV/HIV, HCV/HIV/HTLV-1/-2 coinfected patients (all p<0.05), and the lowest HCV VL was detected in HCV/HTLV-2 coinfected patients. Curiously, 61.1% of the patients with HBV/HTLV-2 coinfection had an undetectable HBV VL at the beginning of the study versus 21.4% in the patients with HBV/HTLV-1 coinfection. Although the percentages of undetectable HCV loads in HCV/HTLV-1 and HCV/HTLV-2 coinfected patients were quite similar, during follow-up, more HCV clearance was detected in patients with HCV/HTLV-2 coinfection [OR 2.65; 95% IC (1.17–5.99)].Major conclusionsHTLV-2 positively impacts HBV and HCV viral loads and HCV clearance, while HIV and/or HTLV-1 negatively impacts HCV viral load. Thus, the search for HTLV-1/-2 in viral hepatitis B and C infected patients has virological prognostic value, which is a strong reason to suggest including HTLV serology in the follow-up of patients.