HIV Virus Infection Research Articles

A promiscuous T cell epitope-based HIV vaccine providing redundant population coverage of the HLA class II elicits broad, polyfunctional T cell responses in nonhuman primates

Over the last few decades, several emerging or reemerging viral diseases with no readily available vaccines have ravaged the world. A platform to fastly generate vaccines inducing potent and durable neutralizing antibody and T cell responses is sorely needed. Bioinformatically identified epitope-based vaccines can focus on immunodominant T cell epitopes and induce more potent immune responses than a whole antigen vaccine and may be deployed more rapidly and less costly than whole-gene vaccines. Increasing evidence has shown the importance of the CD4+ T cell response in protection against HIV and other viral infections. The previously described DNA vaccine HIVBr18 encodes 18 conserved, promiscuous epitopes binding to multiple HLA-DR-binding HIV epitopes amply recognized by HIV-1-infected patients. HIVBr18 elicited broad, polyfunctional, and durable CD4+and CD8+ T cell responses in BALB/c and mice transgenic to HLA class II alleles, showing cross-species promiscuity. To fully delineate the promiscuity of the HLA class II vaccine epitopes, we assessed their binding to 34 human class II (HLA-DR, DQ, and -DP) molecules, and immunized nonhuman primates. Results ascertained redundant 100% coverage of the human population for multiple peptides. We then immunized Rhesus macaques with HIVBr18 under in vivo electroporation. The immunization induced strong, predominantly polyfunctional CD4+ T cell responses in all animals to 13 out of the 18 epitopes; T cells from each animal recognized 7–11 epitopes. Our results provide a preliminary proof of concept that immunization with a vaccine encoding epitopes with high and redundant coverage of the human population can elicit potent T cell responses to multiple epitopes, across species and MHC barriers. This approach may facilitate the rapid deployment of immunogens eliciting cellular immunity against emerging infectious diseases, such as COVID-19.

Piecewise differentiation of the fractional order CAR-T cells-SARS-2 virus model

The pandemic caused by the SARS-CoV2 virus has prompted research into new therapeutic solutions that can be used to treat the CoVid-19 syndrome. As part of this research, immunotherapy, first developed against cancer, is offering new therapeutic horizons also against viral infections. CAR technology, with the production of CAR-T cells (adoptive immunotherapy), has shown applicability in the field of HIV viral infections through second generation CAR-T cells implemented with the “CD4CAR” system with a viral fusion inhibitor. In addition, to avoid the immunoescape of the virus, bi- or trispecific CAR receptors have been developed. Our research group hypothesizes the use of this immunotherapy system against SARS-CoV2, admitting the appropriate adjustments concerning the target-epitope and a possible remodeling of the nuclease related to the action of this virus. For a more in-depth analysis of this hypothesis, a mathematical model has been developed which, starting from the fractional derivative Caputo, creates a system of equations that describes the interactions between CAR-T cells, memory cells, and cells infected with SARS-CoV2. Through an analysis of the existence and non-negativity of the solutions, the hypothesis is stabilized; then is further demonstrated through the use of the piece-wise derivative and the consequent application of the formula of Newton polynomial interpolation.

S2796 Warm Autoimmune Hemolytic Anemia Secondary to Acute Hepatitis B Virus Infection

Introduction: Autoimmune hemolytic anemia (AIHA) is a rare extrahepatic manifestation, typically associated with HIV, hepatitis C, E, and Epstein Barr virus (EBV) infections. Hepatitis B virus (HBV) induced AIHA is an unusual association, not previously described in the literature. We report the first case of HBV-induced warm-AIHA, successfully treated with corticosteroids and anti-viral therapy. Case Description/Methods: A 67-year-old man presented to our hospital with one month of myalgias, arthralgias, and fatigue. He had no known history of the lymphoproliferative disorder, autoimmune disease, immunodeficiency, malignancy, or alcohol abuse. He lived in the woods and reported previous tick exposure and recent unprotected sexual encounters with multiple intravenous drug users. His physical examination revealed mild scleral icterus. Laboratory workup was notable for hemoglobin (Hb) 12.5 gm/dL, reticulocyte count 4.1%, elevated aspartate aminotransferase 493 units/L, alanine aminotransferase 693 units/L, total bilirubin 5.3mg/dL with indirect bilirubinemia 2.4 mg/dL, lactate dehydrogenase 1,158 units/L, and undetectable haptoglobin. Immunohematologic studies showed a direct antiglobulin test positive for IgG and C3 with isolation of warm autoantibodies by elution, consistent with a diagnosis of warm AIHA. Workup to elucidate the cause of AIHA including ANA, anti-proteinase-3, myeloperoxidase antibodies, peripheral blood smear, malaria smear, northeast tick panel, serum protein electrophoresis, and immunofixation were unrevealing. HIV, hepatitis A, C, E, and EBV infections were ruled out. HBV serologies revealed positive HBs-antigen, anti-HBc IgM, and PCR quantification HBV DNA 824,000,000 IU/ml, consistent with acute HBV infection. A diagnosis of warm AIHA secondary to acute HBV infection was made. 1mg/kg/day of prednisone and Tenofovir 25 mg/day were started. During the hospitalization, his anemia worsened, reaching a Hb nadir of 5.2 gm/dl and requiring ten units of packed red blood cell transfusions. He eventually stabilized at day 18, followed by a sustained virological response, clinical and laboratory remission of AIHA. Discussion: This case highlights AIHA as an unusual manifestation of acute HBV infection. An association between AIHA and hepatic viruses, including HIV, HCV, and EBV, has been well recognized. Acute HBV infection induced AIHA has not been reported in the literature yet. Therefore, clinicians should consider HBV infection in any patient presenting with new-onset AIHA of unclear etiology.Figure 1.: The patient's jaundice on physical exam.

Specific Deubiquitinating Enzymes Promote Host Restriction Factors Against HIV/SIV Viruses.

Hijacking host ubiquitin pathways is essential for the replication of diverse viruses. However, the role of deubiquitinating enzymes (DUBs) in the interplay between viruses and the host is poorly characterized. Here, we demonstrate that specific DUBs are potent inhibitors of viral proteins from HIVs/simian immunodeficiency viruses (SIVs) that are involved in viral evasion of host restriction factors and viral replication. In particular, we discovered that T cell-functioning ubiquitin-specific protease 8 (USP8) is a potent and specific inhibitor of HIV-1 virion infectivity factor (Vif)-mediated apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3)G (A3G) degradation. Ectopic expression of USP8 inhibited Vif-induced A3G degradation and suppressed wild-type HIV-1 infectivity even in the presence of Vif. In addition, specific DUBs repressed Vpr-, Vpu-, and Vpx-triggered host restriction factor degradation. Our study has revealed a previously unrecognized interplay between the host’s DUBs and viral replication. Enhancing the antiviral activity of DUBs therefore represents an attractive strategy against HIVs/SIVs.

CUL5-ARIH2 E3-E3 ubiquitin ligase structure reveals cullin-specific NEDD8 activation

An emerging mechanism of ubiquitylation involves partnering of two distinct E3 ligases. In the best-characterized E3-E3 pathways, ARIH-family RING-between-RING (RBR) E3s ligate ubiquitin to substrates of neddylated cullin-RING E3s. The E3 ARIH2 has been implicated in ubiquitylation of substrates of neddylated CUL5-RBX2-based E3s, including APOBEC3-family substrates of the host E3 hijacked by HIV-1 virion infectivity factor (Vif). However, the structural mechanisms remained elusive. Here structural and biochemical analyses reveal distinctive ARIH2 autoinhibition, and activation on assembly with neddylated CUL5-RBX2. Comparison to structures of E3-E3 assemblies comprising ARIH1 and neddylated CUL1-RBX1-based E3s shows cullin-specific regulation by NEDD8. Whereas CUL1-linked NEDD8 directly recruits ARIH1, CUL5-linked NEDD8 does not bind ARIH2. Instead, the data reveal an allosteric mechanism. NEDD8 uniquely contacts covalently linked CUL5, and elicits structural rearrangements that unveil cryptic ARIH2-binding sites. The data reveal how a ubiquitin-like protein induces protein-protein interactions indirectly, through allostery. Allosteric specificity of ubiquitin-like protein modifications may offer opportunities for therapeutic targeting.

Anti-HIV Effects of Baculiferins Are Regulated by the Potential Target Protein DARS.

Baculiferins are a group of marine sponge-derived polycyclic alkaloids with anti-HIV (human immunodeficiency virus) activities. To identify additional baculiferin-based congeners for SAR analysis and to investigate the mode of action, a total of 18 new baculiferin-type derivatives were synthesized. The inhibitory activities of the congeners against the HIV-1 virus were evaluated in vitro, and the relevant SAR was discussed. Compound 18 exerted the most potent activity toward VSV-G-pseudotyped HIV-1 (IC50 of 3.44 μM) and HIV-1 strain SF33 (IC50 of 2.80 μM) in vitro. To identify the cellular targets, three photoaffinity baculiferin probes were simultaneously synthesized. Photoaffinity labeling experiments together with LC-MS/MS data identified aspartate-tRNA ligase (DARS) as a putative target protein of 18. The overexpression and knockdown of DARS in HEK293T cells provided additional data to demonstrate that DARS is a potential target protein in the regulation of HIV virus infection. The modes of antiviral baculiferins 13 and 18 binding to DARS were determined by a molecular docking simulation. Thus, baculiferin 18 is considered a promising lead as a new molecular target for the development of anti-HIV agents.

FORMULATION AND OPTIMIZATION OF RITONAVIR NASAL NANOSUSPENSION FOR BRAIN TARGETING

Nowadays, HIV associated neurological disorder especially HIV-1 virus infection is enhanced. Current available HIV therapies only reduce the plasma viral level and do not kill the virus completely. Administered dosage form does not reach the central nervous system (CNS) completely by the conventional approach. The oral route of drug administration,causes gastrointestinal irritation, hepatic metabolism and slow onset of action and some methods are invasive, resulting in the patient's non compliance. To overcome these problems, an effective novel formulation that will directly reach the CNS or brain needs to be developed.This study aims to formulate intranasal nanosuspension of ritonavir. Ritonavir is widely used as an antiretroviral agent and it is a protease enzyme inhibitor which is poorly soluble in water. High pressure homogenization technique was used for preparation prepare and optimization of nanosuspension by using 2 factors 3 level full factorial design, which is further characterized for particle size, polydispersity index, zeta potential, pH, drug content, in vitro drug diffusion and ex vivo permeation study. For stability of nanosuspension, lyophilization of optimized formulation was done. A comparison study between plain drug, nanosuspension and the lyophilized formulation was carried out, and it showed a significant increase in drug release from the membrane.

Lessons from the Pandemic

Lessons from the Pandemic

Degradation-Independent Inhibition of APOBEC3G by the HIV-1 Vif Protein.

The ubiquitin–proteasome system plays an important role in the cell under normal physiological conditions but also during viral infections. Indeed, many auxiliary proteins from the (HIV-1) divert this system to its own advantage, notably to induce the degradation of cellular restriction factors. For instance, the HIV-1 viral infectivity factor (Vif) has been shown to specifically counteract several cellular deaminases belonging to the apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC3 or A3) family (A3A to A3H) by recruiting an E3-ubiquitin ligase complex and inducing their polyubiquitination and degradation through the proteasome. Although this pathway has been extensively characterized so far, Vif has also been shown to impede A3s through degradation-independent processes, but research on this matter remains limited. In this review, we describe our current knowledge regarding the degradation-independent inhibition of A3s, and A3G in particular, by the HIV-1 Vif protein, the molecular mechanisms involved, and highlight important properties of this small viral protein.

Using the antibody-antigen binding interface to train image-based deep neural networks for antibody-epitope classification.

High-throughput B-cell sequencing has opened up new avenues for investigating complex mechanisms underlying our adaptive immune response. These technological advances drive data generation and the need to mine and analyze the information contained in these large datasets, in particular the identification of therapeutic antibodies (Abs) or those associated with disease exposure and protection. Here, we describe our efforts to use artificial intelligence (AI)-based image-analyses for prospective classification of Abs based solely on sequence information. We hypothesized that Abs recognizing the same part of an antigen share a limited set of features at the binding interface, and that the binding site regions of these Abs share share common structure and physicochemical property patterns that can serve as a "fingerprint" to recognize uncharacterized Abs. We combined large-scale sequence-based protein-structure predictions to generate ensembles of 3-D Ab models, reduced the Ab binding interface to a 2-D image (fingerprint), used pre-trained convolutional neural networks to extract features, and trained deep neural networks (DNNs) to classify Abs. We evaluated this approach using Ab sequences derived from human HIV and Ebola viral infections to differentiate between two Abs, Abs belonging to specific B-cell family lineages, and Abs with different epitope preferences. In addition, we explored a different type of DNN method to detect one class of Abs from a larger pool of Abs. Testing on Ab sets that had been kept aside during model training, we achieved average prediction accuracies ranging from 71-96% depending on the complexity of the classification task. The high level of accuracies reached during these classification tests suggests that the DNN models were able to learn a series of structural patterns shared by Abs belonging to the same class. The developed methodology provides a means to apply AI-based image recognition techniques to analyze high-throughput B-cell sequencing datasets (repertoires) for Ab classification.

N6-methyladenosine modification of HIV-1 RNA suppresses type-I interferon induction in differentiated monocytic cells and primary macrophages.

N6-methyladenosine (m6A) is a prevalent RNA modification that plays a key role in regulating eukaryotic cellular mRNA functions. RNA m6A modification is regulated by two groups of cellular proteins, writers and erasers that add or remove m6A, respectively. HIV-1 RNA contains m6A modifications that modulate viral infection and gene expression in CD4+ T cells. However, it remains unclear whether m6A modifications of HIV-1 RNA modulate innate immune responses in myeloid cells that are important for antiviral immunity. Here we show that m6A modification of HIV-1 RNA suppresses the expression of antiviral cytokine type-I interferon (IFN-I) in differentiated human monocytic cells and primary monocyte-derived macrophages. Transfection of differentiated monocytic U937 cells with HIV-1 RNA fragments containing a single m6A-modification significantly reduced IFN-I mRNA expression relative to their unmodified RNA counterparts. We generated HIV-1 with altered m6A levels of RNA by manipulating the expression of the m6A erasers (FTO and ALKBH5) or pharmacological inhibition of m6A addition in virus-producing cells, or by treating HIV-1 RNA with recombinant FTO in vitro. HIV-1 RNA transfection or viral infection of differentiated U937 cells and primary macrophages demonstrated that HIV-1 RNA with decreased m6A levels enhanced IFN-I expression, whereas HIV-1 RNA with increased m6A modifications had opposite effects. Our mechanistic studies indicated that m6A of HIV-1 RNA escaped retinoic acid-induced gene I (RIG-I)-mediated RNA sensing and activation of the transcription factors IRF3 and IRF7 that drive IFN-I gene expression. Together, these findings suggest that m6A modifications of HIV-1 RNA evade innate immune sensing in myeloid cells.

Advances in Nucleoside and Nucleotide Analogues in Tackling Human Immunodeficiency Virus and Hepatitis Virus Infections.

Nucleoside and nucleotide analogues are structurally similar antimetabolites and are promising small-molecule chemotherapeutic agents against various infectious DNA and RNA viruses. To date, these analogues have not been documented in-depth as anti-human immunodeficiency virus (HIV) and anti-hepatitis virus agents, these are at various stages of testing ranging from pre-clinical, to those withdrawn from trials, or those that are approved as drugs. Hence, in this review, the importance of these analogues in tackling HIV and hepatitis virus infections is discussed with a focus on the viral genome and the mechanism of action of these analogues, both in a mutually exclusive manner and their role in HIV/hepatitis coinfection. This review encompasses nucleoside and nucleotide analogues from 1987 onwards, starting with the first nucleoside analogue, zidovudine, and going on to those in current clinical trials and even the drugs that have been withdrawn. This review also sheds light on the prospects of these nucleoside analogues in clinical trials as a treatment option for the COVID-19 pandemic.

Generation of HIV-resistant cells with a single-domain antibody: implications for HIV-1 gene therapy

The cure or functional cure of the “Berlin patient” and “London patient” indicates that infusion of HIV-resistant cells could be a viable treatment strategy. Very recently, we genetically linked a short-peptide fusion inhibitor with a glycosylphosphatidylinositol (GPI) attachment signal, rendering modified cells fully resistant to HIV infection. In this study, GPI-anchored m36.4, a single-domain antibody (nanobody) targeting the coreceptor-binding site of gp120, was constructed with a lentiviral vector. We verified that m36.4 was efficiently expressed on the plasma membrane of transduced TZM-bl cells and targeted lipid raft sites without affecting the expression of HIV receptors (CD4, CCR5, and CXCR4). Significantly, TZM-bl cells expressing GPI-m36.4 were highly resistant to infection with divergent HIV-1 subtypes and potently blocked HIV-1 envelope-mediated cell-cell fusion and cell-cell viral transmission. Furthermore, we showed that GPI-m36.4-modified human CEMss-CCR5 cells were nonpermissive to both CCR5- and CXCR4-tropic HIV-1 isolates and displayed a strong survival advantage over unmodified cells. It was found that GPI-m36.4 could also impair HIV-1 Env processing and viral infectivity in transduced cells, underlying a multifaceted mechanism of antiviral action. In conclusion, our studies characterize m36.4 as a powerful nanobody that can generate HIV-resistant cells, offering a novel gene therapy approach that can be used alone or in combination.

Hodgkin’s Lymphoma in HIV-Infected Patients

Aim. To assess clinical and laboratory characteristics of the unique category of HIV-positive patients with hepatitis C or B co-infection combined with Hodgkin’s lymphoma (HL). Materials & Methods. The paper provides data on 85 HIV-positive patients with HL followed-up at the Department of Hematology and Secondary Immunodeficiencies of the AS Loginov Moscow Clinical Scientific Center from 2002 to 2019 (data on 2008-2010 are not available). The distribution of patients by sex was approximately equal, median age was 35 years (range 20-74 years). Results. Histological HL variant is predominantly mixedcell with many positive tests for Epstein-Barr virus. More than 80 % of patients with concomitant HIV infection were admitted to the AS Loginov Center with HL stage III/IV. Most of them received highly active anti-retroviral therapy (HAART) before HL diagnosis. The distinguishing feature of HIV-positive patients with HL appeared to be high (as compared to HIV patients with other lymphoma variants) CD4+ lymphocyte count. This phenomenon is considered within the framework of immune reconstitution inflammatory syndrome (IRIS). A clue to this phenomenon may lay the foundation in addressing the issue of lymphoma genesis and development. Viral load was moderate and undetectable. Hepatitis C and/or B co-infection was identified in 95 % of patients. Antiviral therapy for concomitant hepatitis C was administered concurrent with HAART. All patients received АBVD, BEACOPP-14, BEACOPP-escalat-ed, DHAP, ESHAP antitumor regimens. Radiotherapy was used if necessary. In hepatitis C HAART and direct-acting drugs were administered concurrent with chemotherapy. No severe adverse reactions were observed. Even before starting antitumor treatment of HL patients with concomitant HIV and/or hepatitis viral infections, mortality was 8 %. But in the group of patients with the same co-infections who received HL chemotherapy, mortality was 10 %. The cause of death was HL stage IVB with viral liver cirrhosis, agranulocytosis, and sepsis. Conclusion. Diseases considered incurable in the past, such as HL and hepatitis C, can be healed today. Compromised immunity of HIV-positive patients can be successfully stabilized with HAART.

Rapid Diagnosis of HIV-1 virus by Near Infrared Spectroscopy: based on Partial least squares regression

Currently, the laboratory diagnostic tests available for HIV-1 viral infection are mainly based on serological testing which relies on enzyme-linked immunosorbent assay (ELISA) for blood HIV antigen detection and reverse transcription polymerase chain reaction (RT-PCR) for HIV specific RNA sequence identification. However, these methods are expensive and time-consuming, and suffer from false positive and/or false negative results. Thus, there is an urgent need for developing a cost effective, rapid and accurate diagnostic method for HIV-1 infection. In order to reduce the barriers for effective diagnosis, a near-infrared spectroscopy (NIR) method was used to detect the HIV-1 virus in human serum, specifically, three absorption peaks with dose-dependent at 1582nm, 1810nm and 2363nm were found by multiple FBiPLSR test analysis for HIV-nano and HIV-EGFP, but not for MLV. Therefore, we recommend the use of 1582nm, 1810nm and 2363nm as the characteristic spectrum peak, for early screening and rapid diagnosis of serum HIV.

The Therapeutic Potential of Spirulina to Combat COVID 19 Infection

MANY countries and labs are currently looking for a COVID-19 vaccine but have yet to explore it. Many species of Spirulina contain significant active compounds such as sulfated polysaccharides, phenols, phycobiliproteins, and calcium spirulan with inhibition activity against replication of viruses, especially influenza A (H1N1), HCV , and HIV viral infection. As there is no vaccine was approved against COVID-19, the potential of using Spirulina as antivirus and an immune agent has been tested for many viruses, and this encourages using the Spirulina as a whole amount or its extract for immunization against COVID-19, the causative pathogen of Coronavirus disease. The present article discusses some of the important studies on the therapeutic antiviral activities of the cyanobacterium Spirulina platensis.

A novel HIV-1 inhibitor that blocks viral replication and rescues APOBEC3s by interrupting vif/CBFβ interaction

HIV remains a health challenge worldwide, partly because of the continued development of resistance to drugs. Therefore, it is urgent to find new HIV inhibitors and targets. Apolipoprotein B mRNA-editing catalytic polypeptide-like 3 family members (APOBEC3) are important host restriction factors that inhibit HIV-1 replication by their cytidine deaminase activity. HIV-1 viral infectivity factor (Vif) promotes proteasomal degradation of APOBEC3 proteins by recruiting the E3 ubiquitin ligase complex, in which core-binding factor β (CBFβ) is a necessary molecular chaperone. Interrupting the interaction between Vif and CBFβ can release APOBEC3 proteins to inhibit HIV-1 replication and may be useful for developing new drug targets for HIV-1. In this study, we identified a potent small molecule inhibitor CBFβ/Vif-3 (CV-3) of HIV-1 replication by employing structure-based virtual screening using the crystal structure of Vif and CBFβ (PDB: 4N9F) and validated CV-3's antiviral activity. We found that CV-3 specifically inhibited HIV-1 replication (IC50 = 8.16 µm; 50% cytotoxic concentration >100 µm) in nonpermissive lymphocytes. Furthermore, CV-3 treatment rescued APOBEC3 family members (human APOBEC3G (hA3G), hA3C, and hA3F) in the presence of Vif and enabled hA3G packaging into HIV-1 virions, which resulted in Gly-to-Ala hypermutations in viral genomes. Finally, we used FRET to demonstrate that CV-3 inhibited the interaction between Vif and CBFβ by simultaneously forming hydrogen bonds with residues Gln-67, Ile-102, and Arg-131 of CBFβ. These findings demonstrate that CV-3 can effectively inhibit HIV-1 by blocking the interaction between Vif and CBFβ and that this interaction can serve as a new target for developing HIV-1 inhibitors.

Multifaceted HIV-1 Vif interactions with human E3 ubiquitin ligase and APOBEC3s.

APOBEC3 (A3) proteins are a family of host antiviral restriction factors that potently inhibit various retroviral infections, including human immunodeficiency virus (HIV)-1. To overcome this restriction, HIV-1 virion infectivity factor (Vif) recruits the cellular cofactor CBFβ to assist in targeting A3 proteins to a host E3 ligase complex for polyubiquitination and subsequent proteasomal degradation. Intervention of the Vif-A3 interactions could be a promising therapeutic strategy to facilitate A3-mediated suppression of HIV-1 in patients. In this structural snapshot, we review the structural features of the recently determined structure of human A3F in complex with HIV-1 Vif and its cofactor CBFβ, discuss insights into the molecular principles of Vif-A3 interplay during the arms race between the virus and host, and highlight the therapeutic implications.

A Rare Case Report of Invasive Ocular Surface Squamous Neoplasm of Conjunctiva

Ocular surface neoplasm(OSSN) represent a rare but broad spectrum of disease, including mild dysplasia on one end of the spectrum and invasive Squamous cell carcinoma(SCC) on the other. Thus, the diagnosis completely depends on histopathological examination of the lesion. The incidence of ocular surface neoplasia is strongly associated with factors like solar ultraviolet radiation, HIV and human papilloma virus(HPV) infections. Most lesions occur at the limbus within the interpalpebral fissure particularly the nasal side. Their importance lies in the fact that they mimic benign lesions like pterygium or even chronic conjunctivitis and thus can be misinterpreted and inadequately treated. Red eye and ocular irritation are the most common presenting symptoms. No tumor related deaths or metastasis are generally seen. Surgery with intra-operative control of surgical margins and adjunctive chemotherapy, immunotherapy and cryotherapy result in good tumor control rates, with promising results in aggressive, recurrent and large tumors.

Knowledge, Attitude and Practice about Hepatitis B, Hepatitis C and Human Immunodeficiency Virus among Barbers of Sylhet, Bangladesh

Introduction:This study was designed to see the knowledge, attitude and practice of barbers regarding transmission of hepatitis B, C and HIV viral infections.
 Materials and Methods: Barbers from Sylhet were interviewed with a predesigned questionnaire. Positive answers for blood transfusion, syringe sharing, use of contaminated shaving instruments and unsafe sex as way of transmission were taken as correct. Statistical analysis was done using SPSS 20 version.
 Result: Total 403 barbers, age from 14 years to 69 years (mean 27.11) were interviewed. In this group 232 (57.6%) had education illiterate to class five level. Among them 245 (60.3%) had income below 10 thousand per month. Blood transfusion could transmit HBV, HCV and HIV was known to 136 (33.7%), 129 (32.00%) and 247 (61.30%), contaminated syringe sharing could transmit HBV, HCV and HIV respectively was known to 131 (32.5%), 127 (31.50%) and 278 (69.0%) barbers, unsafe sex could transmit HBV, HCV and HIV was known to 166 (41.2%), 158(39.2%) and 317 (78.70%) barbers respectively and Contaminated shaving instruments could transmit HBV, HCV and HIV was known to 101 (25.1%), 96 (23.8%) and 156 (38.7%) barbers respectively. In this series 84 (20.84%) barbers answered correctly. This answers differed significantly within different level of education. Their knowledge of sterilization of shaving instruments was poor.
 Conclusion: Knowledge of our barbers regarding transmission of HBV, HCV and HIV and sterilisatioin of shaving instruments are inadequate. Institutional education and structured professional training may improve their services and decrease transmission of blood borne viral diseases.
 Medicine Today 2020 Vol.32(2): 117-121