An insight into fruit aroma volatilome during postharvest maturation in two popular Musa cultivars of tropics.

BACKGROUND: Banana is one of the major global horticultural fruit crops cultivated in the humid tropics and subtropics. Fruit quality and consumer acceptability of any climacteric fruit depend mainly on its postharvest aroma volatile profiles. The present study aimed to profile fruit volatiles status during postharvest storage of two banana cultivars: Kanthali (Musa sp. cv. Kanthali, Kt) and Kacha Kela (Musa sp. cv. Kacha Kela, Kk) from the ABB genome group. RESULTS: Both cultivars showed differences in the soluble sugar contents, with Kt being higher than Kk. The volatile compounds were profiled from the pulp as emitted, endogenous and glycosyl-bound forms, along with peel-endogenous and whole fruit volatiles during postharvest storage. Both cultivars showed a wide range of variations in volatile aroma pools; nevertheless, esters and aliphatic compounds were found to be the major contributors of fruit volatiles in Kt and Kk, respectively. The pulp-endogenous volatiles served as the major pool, which showed a sharp decline with a corresponding increase of emission. Many volatiles were found to be glycosylated during early postharvest storage, with de-glycosylation occurring with an increase in storage time, resulting in fruit softening and a concurrent supply of sugar bound volatiles towards emission. CONCLUSION: As a whole, the study outcome provides an overview of fruit volatilome during postharvest storage and suggests a possible inter-linking among the volatile components in the cultivars. It is plausible that the release of aroma volatiles from pulp is mediated via peel, with volatiles accumulating as peel-endogenous volatiles representing the temporary pool reservoir. © 2022 Society of Chemical Industry.

Anti-hepatitis B virus (HBV) response of imiquimod based toll like receptor 7 ligand in hbv-positive human hepatocelluar carcinoma cell line.

BACKGROUND: Toll like receptors (TLRs) play an important role in innate immunity and various studies suggest that TLRs play a crucial role in pathogenesis of hepatitis B virus (HBV) infection. The present study aims in looking into the status of crucial host and viral gene expression on inciting TLR7. METHODS: The transcription of TLR7 pathway signaling molecules and HBV DNA viral load were quantified by Real Time-PCR after stimulation of TLR7 with its imiquimod based ligand, R837. Cell cycle analysis was performed using flow-cytometry. Expression of TLR7 and chief cell cycle regulator governing G1/S transition, p53 was also seen in liver biopsysss samples of CHB patients. HBV induced alteration in histone modifications in HepG2 cells and its restoration on TLR7 activation was determined using western blot. RESULTS: The TLR7 expression remains downregulated in HepG2.2.15 cells and in liver biopsy samples from CHB patients. Interestingly HBV DNA viral load showed an inverse relationship with the TLR7 expression in the biopsy samples. We also evaluated the anti-viral activity of R837, an agonist of TLR7. It was observed that there was a suppression of HBV replication and viral protein production upon TLR7 stimulation. R837 triggers the anti-viral action probably through the Jun N-terminal Kinase (JNK) pathway. We also observed a downregulation of histone H3K9Me3 repression mark upon R837 treatment in HBV replicating HepG2.2.15 cells, mimicking that of un-infected HepG2 cells. Additionally, the G1/S cell cycle arrest introduced by HBV in HepG2.2.15 cells was released upon ligand treatment. CONCLUSION: The study thus holds a close insight into the changes in hepatocyte micro-environment on TLR7 stimulation in HBV infection.

Tumor suppressor micro RNA miR-145 and onco micro RNAs miR-21 and miR-222 expressions are differentially modulated by hepatitis B virus X protein in malignant hepatocytes.

BACKGROUND: Hepatitis B Virus (HBV) X protein (HBx) is known to be involved in the initiation and progression of hepatocellular carcinoma (HCC) through modulation of host gene response. Alterations in miRNA expressions are frequently noted in HCC. This study is aimed to examine the role of HBx protein in the modulation of oncogenic miRNA-21, miRNA-222 and tumor suppressor miRNA-145 in malignant hepatocytes. METHODS: Expressions of miRNA-21, miRNA-222 and miRNA-145 were measured in HepG2 cells transfected with HBx-plasmid (genotype D) and with full length HBV genome (genotype D) and also in stably HBV producing HepG2.2.15 cells using real time PCR. Their target mRNAs and proteins - PTEN, p27 and MAP3K - were analyzed by real time PCR and western blot respectively. miRNA expressions were measured after HBx/D mRNA specific siRNA treatment. The expressions of these miRNAs were analyzed in liver cirrhosis and HCC patients also. RESULTS: The study revealed a down-regulation of miRNA-21 and miRNA-222 expressions in HBx transfected HepG2 cells, pUC-HBV 1.3 plasmid transfected HepG2 cells as well as in HepG2.2.15 cells. Down regulation of miRNA-21 and miRNA-222 expression was observed in patient serum samples. Down regulation of miRNA-145 expression was observed in HepG2 cells transiently transfected with HBx and pUC-HBV1.3 plasmid as well as in patient samples but the expression of miRNA-145 was increased in HepG2.2.15 cells. Target mRNA and protein expressions were modulated in HepG2 cells and in HepG2.2.15 cell line consistent with the modulation of miRNA expressions. CONCLUSION: Thus, HBx protein differentially modulated the expression of miRNAs. The study throws light into possible way by which HBx protein acts through microRNA and thereby regulates host functioning. It might suggest new therapeutic strategies against hepatic cancer.

Cellular states are coupled to genomic and viral heterogeneity in HPV-related oropharyngeal carcinoma.

Head and neck squamous cell carcinoma (HNSCC) includes a subset of cancers driven by human papillomavirus (HPV). Here we use single-cell RNA-seq to profile both HPV-positive and HPV-negative oropharyngeal tumors, uncovering a high level of cellular diversity within and between tumors. First, we detect diverse chromosomal aberrations within individual tumors, suggesting genomic instability and enabling the identification of malignant cells even at pathologically negative margins. Second, we uncover diversity with respect to HNSCC subtypes and other cellular states such as the cell cycle, senescence and epithelial-mesenchymal transitions. Third, we find heterogeneity in viral gene expression within HPV-positive tumors. HPV expression is lost or repressed in a subset of cells, which are associated with a decrease in HPV-associated cell cycle phenotypes, decreased response to treatment, increased invasion and poor prognosis. These findings suggest that HPV expression diversity must be considered during diagnosis and treatment of HPV-positive tumors, with important prognostic ramifications.

Epithelial-Mesenchymal Plasticity in Tumor Immune Evasion.

Epithelial-mesenchymal transition (EMT) is a fundamental process that occurs during embryogenesis and tissue repair. However, EMT can be hijacked by malignant cells, where it may promote immune evasion and metastasis. Classically considered a dichotomous transition, EMT in cancer has recently been considered a plastic process whereby malignant cells display and interconvert among hybrid epithelial/mesenchymal (E/M) states. Epithelial-mesenchymal plasticity (EMP) and associated hybrid E/M states are divergent from classical EMT, with unique immunomodulatory effects. Here, we review recent insights into the EMP-immune cross-talk, highlighting possible mechanisms of immune evasion conferred by hybrid E/M states and roles of immune cells in EMP.

Identification and Genomic Characterization of Parvovirus B19V Genotype 3 Viruses from Cases of Meningoencephalitis in West Bengal, India.

Brain infections are a major public health problem in India and other parts of the world, causing both mortality and lifelong disability. Even after a thorough investigation, many cases remain without an etiological diagnosis. Primate erythroparvovirus 1 (B19V) has been identified as a pathogen associated with undiagnosed meningoencephalitis in other settings, including the United Kingdom, France, and Latvia. Here, we reported 13/403 (3.2%) B19V PCR positive cases of meningoencephalitis in West Bengal, India. The positive samples were mostly from children (10/13, 76.92%) and presented as a spectrum consisting of acute encephalitis (7/13), acute meningoencephalitis (3/13), and meningitis (3/13). Of the 13 cases, 8/13 (61.5%) had no known etiology and 5/13 (38.5%) had a previous etiological diagnosis. The cases did not cluster in time or by location, suggesting sporadic occurrence rather than outbreaks. We were able to retrieve the complete B19V genomes from cerebrospinal fluid (CSF) in 12/13 cases. The sequences clustered into genotype 3b with complete genomes from Brazil, Ghana, and France, and partial genomes from India and Kyrgyzstan. This is the first report of B19V in cases of neurological infections from India. It highlights the need to evaluate the causal relationship between B19V with meningoencephalitis in the country. These were also the first complete genomes of genotype 3b from CSF and will be critical in the evaluation of the relationship between genotypes and disease. IMPORTANCE Cases of meningoencephalitis with no known etiology remain a major challenge to clinical management of brain infections across the world. In this study, we detected and characterized the whole-genome of primate erythroparvovirus 1 (B19V) in cases of meningoencephalitis in India. Our work highlighted the association between B19V and brain infections which has been reported in other countries. Our work also emphasized the need to examine the role of B19V in meningoencephalitis, specifically whether it caused or contributed to the disease together with other pathogens in India. Our study provided the first 12 genomes of B19V from cerebrospinal fluid. These genomes will contribute to an understanding of how the virus is changing across different locations and over time.

Discriminatory behavior of a rhodamine 6G decorated mesoporous silica based multiple cation sensor towards Cu2+ and Hg2+vis-à-vis Al3+, Cr3+ and Fe3+: selective removal of Cu2+ and Hg2+ from aqueous media.

Selective identification of metal ions as well as their removal is possible when a sensing unit is anchored to a solid support. In this paper, functionalized mesoporous silica with a pendant rhodamine 6G moiety (R6FMS) has been obtained by successive grafting of an aldehyde derivative of bisphenol A followed by rhodamine 6G over a 3-aminopropyl anchored mesoporous silica framework. The materials have been characterized by powder X-ray diffraction, nitrogen sorption and electron microscopy studies, FT-IR and solid state MAS NMR spectral studies, and thermal analysis. In ethanol, the colorless silica material gives pink coloration in the presence of Al3+, Cr3+, Fe3+ and Cu2+ which is also clearly evident from the generation of an absorption peak at 525 nm. Upon excitation at 500 nm, the fluorescence intensity of the probe increases by 36-, 17-, 40- and 89-fold in the presence of Al3+, Cr3+, Fe3+ and Cu2+ ions, respectively. This suggests that R6FMS is a colorimetric and fluorescent chemosensor for these cations in ethanol. However, when the solvent is changed from ethanol to water, it becomes a selective chemosensor only for Cu2+ and Hg2+, by the generation of a pink color and strong fluorescence at ca. 550 nm, thereby discriminating the trivalent cations. Cations induce the opening of the spirolactam ring resulting in pink coloration and strong fluorescence. The quantum yield and lifetime of the probe have been increased considerably in the presence of these cations in ethanol as well as in aqueous media. The detection limit values for these cations range from 10-6 to 10-8 M. R6FMS has been used to remove Hg2+ and Cu2+ from their aqueous solution with a maximum adsorption capacity of 35 mg g-1 and 148 mg g-1 for Cu2+ and Hg2+, respectively.

Partial EMT in head and neck cancer biology: a spectrum instead of a switch.

Our understanding of epithelial-to-mesenchymal transition (EMT) has slowly evolved from a simple two state, binary model to a multi-step, dynamic continuum of epithelial-to-mesenchymal plasticity, with metastable intermediate transition states that may drive cancer metastasis. Head and neck cancer is no exception, and in this review, we use head and neck as a case study for how partial-EMT (p-EMT) cell states may play an important role in cancer progression. In particular, we summarize recent in vitro and in vivo studies that uncover these intermediate transition states, which exhibit both epithelial and mesenchymal properties and appear to have distinct advantages in migration, survival in the bloodstream, and seeding and propagation within secondary metastatic sites. We then summarize the common and distinct regulators of p-EMT as well as methodologies for identifying this unique cellular subpopulation, with a specific emphasis on the role of cutting-edge technologies, such as single cell approaches. Finally, we propose strategies to target p-EMT cells, highlighting potential opportunities for therapeutic intervention to specifically target the process of metastasis. Thus, although significant challenges remain, including numerous gaps in current knowledge, a deeper understanding of EMT plasticity and a genuine identification of EMT as spectrum rather than a switch will be critical for improving patient diagnosis and treatment across oncology.

Supercapacitor behaviour of manganese dioxide decorated mesoporous silica synthesized by a rapid sol-gel inverse micelle method.

A new type of mesoporous silica (MS) with high surface area and large pore volume has been synthesised by employing a rapid sol-gel based inverse micelle method and electrochemically active metal center, manganese, has been incorporated into it. The MnO2 decorated silica composites are obtained through the wet impregnation technique using KMnO4 followed by their reduction under neutral conditions. The structure and surface area of the samples have been characterised by powder X-ray diffraction (XRD), BET surface area and pore size analysis, transmission and scanning electron microscopy (TEM and FE-SEM), FT-IR spectroscopy and X-ray photoelectron spectroscopy (XPS). Electrochemical techniques, i.e. cyclic voltammetry (CV), galvanostatic charge-discharge (GCD) and electrochemical impedance spectroscopy (EIS), have been used to evaluate the electrochemical properties of the composites. The resultant composite MS/MnO2-3 with a significantly high surface area (453 m2 g-1) is found to exhibit a superior specific capacitance of 1158.50 F g-1 at a scan rate of 5 mV s-1 which is very close to the theoretical value and retains 87.8% of its capacitance up to 1000 cycles at 1 A g-1 current density. The outstanding electrochemical performance of the composite can be attributed to the high surface area and uniform pore size distribution of the novel silica host which simultaneously increases the electrochemically active centres, promotes electrolyte penetration and enhances electron transport. The simplicity of the synthesis process developed here is interesting for wide-scale production of MnO2-based electro-active materials.

EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma.

Wnt signaling is downregulated in embryonal rhabdomyosarcoma (ERMS) and contributes to the block of differentiation. Epigenetic mechanisms leading to its suppression are unknown and could pave the way toward novel therapeutic modalities. We demonstrate that EHMT2 suppresses canonical Wnt signaling by activating expression of the Wnt antagonist DKK1. Inhibition of EHMT2 expression or activity in human ERMS cell lines reduced DKK1 expression and elevated canonical Wnt signaling resulting in myogenic differentiation in vitro and in mouse xenograft models in vivo. Mechanistically, EHMT2 impacted Sp1 and p300 enrichment at the DKK1 promoter. The reduced tumor growth upon EHMT2 deficiency was reversed by recombinant DKK1 or LGK974, which also inhibits Wnt signaling. Consistently, among 13 drugs targeting chromatin modifiers, EHMT2 inhibitors were highly effective in reducing ERMS cell viability. Our study demonstrates that ERMS cells are vulnerable to EHMT2 inhibitors and suggest that targeting the EHMT2-DKK1-ß-catenin node holds promise for differentiation therapy.

Genetics, epigenetics and redox homeostasis in rhabdomyosarcoma: Emerging targets and therapeutics.

Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma accounting for 5-8% of malignant tumours in children and adolescents. Children with high risk disease have poor prognosis. Anti-RMS therapies include surgery, radiation and combination chemotherapy. While these strategies improved survival rates, they have plateaued since 1990s as drugs that target differentiation and self-renewal of tumours cells have not been identified. Moreover, prevailing treatments are aggressive with drug resistance and metastasis causing failure of several treatment regimes. Significant advances have been made recently in understanding the genetic and epigenetic landscape in RMS. These studies have identified novel diagnostic and prognostic markers and opened new avenues for treatment. An important target identified in high throughput drug screening studies is reactive oxygen species (ROS). Indeed, many drugs in clinical trials for RMS impact tumour progression through ROS. In light of such emerging evidence, we discuss recent findings highlighting key pathways, epigenetic alterations and their impacts on ROS that form the basis of developing novel molecularly targeted therapies in RMS. Such targeted therapies in combination with conventional therapy could reduce adverse side effects in young survivors and lead to a decline in long-term morbidity.

A fixed intraoral nail biting habit-breaker appliance: A case report of a novel approach to prevent onychophagia.

Onychophagia or nail biting is the performance of repetitive actions of biting one's nails often to the level of mutilation of the nail beds. It is a compulsive act most often seen in adolescents but may continue into adulthood, leading to deleterious consequences. Often spurred by anxiety and stress, this oral habit is not so readily addressed by patients and in turn not very much treated by dentists or physicians. This case report describes successful treatment of an adolescent patient with a nail biting habit, with an innovative intraoral fixed habit-breaker appliance.

Mesoporous silica based recyclable probe for colorimetric detection and separation of ppb level Hg2+ from aqueous medium.

Functional mesoporous silica probes, MCM-TFM and SBA-TFM, have been synthesized with varying pore sizes and having S-donor sites judiciously selected to bind soft metal centers. The soft S-donor centers are contributed by the thiol functional groups that are introduced into the silica matrices by functionalization with tris(4-formylphenyl)amine followed by 2-aminothiophenol. The materials rapidly and selectively detect Hg2+ colorimetrically and the change in color profile can be perceived through bare eyes. The probes can decontaminate the pollutant heavy metal from aqueous medium at ppb level and the materials are recyclable and reusable for several separation cycles.

Stressing the (Epi)Genome: Dealing with Reactive Oxygen Species in Cancer.

SIGNIFICANCE: Growing evidence indicates cross-talk between reactive oxygen species (ROS) and several key epigenetic processes such as DNA methylation, histone modifications, and miRNAs in normal physiology and human pathologies including cancer. This review focuses on how ROS-induced oxidative stress, metabolic intermediates, and epigenetic processes influence each other in various cancers. Recent Advances: ROS alter chromatin structure and metabolism that impact the epigenetic landscape in cancer cells. Several site-specific DNA methylation changes have been identified in different cancers and are discussed in the review. We also discuss the interplay of epigenetic enzymes and miRNAs in influencing malignant transformation in an ROS-dependent manner. CRITICAL ISSUES: Loss of ROS-mediated signaling mostly by epigenetic regulation may promote tumorigenesis. In contrast, augmented oxidative stress because of high ROS levels may precipitate epigenetic alterations to effect various phases of carcinogenesis. We address both aspects in the review. FUTURE DIRECTIONS: Several drugs targeting ROS are under various stages of clinical development. Recent analysis of human cancers has revealed pervasive deregulation of the epigenetic machinery. Thus, a better understanding of the cross-talk between ROS and epigenetic alterations in cancer could lead to the identification of new drug targets and more effective treatment modalities.

A drive in SUVs: From development to disease.

Progression of cells through distinct phases of the cell cycle, and transition into out-of-cycling states, such as terminal differentiation and senescence, is accompanied by specific patterns of gene expression. These cell fate decisions are mediated not only by distinct transcription factors, but also chromatin modifiers that establish heritable epigenetic patterns. Lysine methyltransferases (KMTs) that mediate methylation marks on histone and non-histone proteins are now recognized as important regulators of gene expression in cycling and non-cycling cells. Among these, the SUV39 sub-family of KMTs, which includes SUV39H1, SUV39H2, G9a, GLP, SETDB1, and SETDB2, play a prominent role. In this review, we discuss their biochemical properties, sub-cellular localization and function in cell cycle, differentiation programs, and cellular senescence. We also discuss their aberrant expression in cancers, which exhibit de-regulation of cell cycle and differentiation.

Occult hepatitis B virus infection in HIV positive patients at a tertiary healthcare unit in eastern India.

Occult HBV infection (OBI), defined by the presence of HBV DNA in absence of hepatitis B surface antigen (HBsAg), is a significant concern in the HIV-infected population. Of 441 HIV+/HBsAg- patients analyzed, the overall prevalence of OBI was 6.3% (28/441). OBI was identified in 21 anti-HBc positives (17.8%), as well as among those who lacked any HBV-specific serological markers (2.2%). Comparison with HIV/HBV co-infection revealed that the levels of CD4, ALT, and HBV DNA were significantly lower during occult infection. Discrete differences were also observed with respect to quasispecies divergence. Additionally, subgenotype D1 was most frequent in occult infection, while D2 was widespread during chronic infection. The majority (~90%) of occult D1 sequences had the sQ129R mutation in the surface gene. This study highlights several distinct features of OBI in India and underscores the need for additional HBV DNA screening in HIV-positive individuals.

High dilutions of a drug of COVID-19 origin show difference in ranks

High dilutions (HDs) of drugs, used in Homeopathy, are prepared in aqueous EtOH (ethanol) through serial dilution accompanying mechanical agitation or succussion, and are called potencies. The potencies from the rank 12 onwards are too dilute to contain any original drug molecules. Do the potency ranks show any difference from each other? Do serial dilution and succussion contribute to the difference in potency ranks? This study aims to address these two questions. The throat swab of a Covid-19 patient was preserved and diluted with aqueous EtOH 90% to prepare the mother tincture (MT) and five different potencies of Covid named Covidinum. These potencies and their solvent media were analysed by electronic and vibrational spectroscopy. Charge transfer (CT) and proton transfer interactions occur during preparation of the potencies. The FT-IR spectra of all the test samples after normalization show difference from each other with respect to O-H stretching and bending (v2) bands. Serial dilution and succussion contribute to the observed difference in ranks and CT interactions.

Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study.

AIM: Toll like receptors plays a significant anti-viral role in different infections. The aim of this study was to look into the role of toll like receptor 4 (TLR4) in hepatitis B virus (HBV) infection. METHODS: Real time PCR was used to analyze the transcription of TLR4 signaling molecules, cell cycle regulators and HBV DNA viral load after triggering the HepG2.2.15 cells with TLR4 specific ligand. Nuclear factor (NF)-κB translocation on TLR4 activation was analyzed using microscopic techniques. Protein and cell cycle analysis was done using Western Blot and FACS respectively. RESULTS: The present study shows that TLR4 activation represses HBV infection. As a result of HBV suppression, there are several changes in host factors which include partial release in G1/S cell cycle arrest and changes in host epigenetic marks. Finally, it was observed that anti-viral action of TLR4 takes place through the NF-κB pathway. CONCLUSION: The study shows that TLR4 activation in HBV infection brings about changes in hepatocyte microenvironment and can be used for developing a promising therapeutic target in future.

Hepatitis B virus X protein mediated suppression of miRNA-122 expression enhances hepatoblastoma cell proliferation through cyclin G1-p53 axis.

BACKGROUND: Hepatitis B virus (HBV) X protein (HBx) reported to be associated with pathogenesis of hepatocellular carcinoma (HCC) and miR-122 expression is down regulated in HCC. Previous studies reported miR-122 targets cyclin G1 (CCNG1) expression and this in turn abolishes p53-mediated inhibition of HBV replication. Here we investigated the involvement of HBx protein in the modulation of miR-122 expression in hepatoblastoma cells. METHODS: Expression of miR-122 was measured in HepG2 cells transfected with HBx plasmid (HBx-HepG2), full length HBV genome (HBV-HepG2) and in constitutively HBV synthesizing HepG2.2.15 cells. CCNG1 mRNA (a direct target of miR-122) and protein expressions were also measured in both HBx-HepG2, HBV-HepG2 cells and in HepG2.2.15 cells. miR-122 expressions were analyzed in HBx-HepG2, HBV-HepG2 and in HepG2.2.15 cells after treatment with HBx mRNA specific siRNA. Expressions of p53 mRNA and protein which is negatively regulated by CCNG1 were analyzed in HBx transfected HepG2 cells; X silenced HBx-HepG2 cells and X silenced HepG2.2.15 cells. HBx induced cell proliferation in HepG2 cells was measured by cell proliferation assay. Flow cytometry was used to evaluate changes in cell cycle distribution. Expression of cell cycle markers were measured by real time PCR. RESULTS: Expression of miR-122 was down regulated in HBx-HepG2, HBV-HepG2 and also in HepG2.2.15 cell line compared to control HepG2 cells. CCNG1 expression was found to be up regulated in HBx-HepG2, HBV-HepG2 cells and in HepG2.2.15 cells. Following siRNA mediated silencing of HBx expression; increased miR-122 levels were documented in HBx-HepG2, HBV-HepG2 and in HepG2.2.15 cells. HBx silencing in HBx-HepG2 and HepG2.2.15 cells also resulted in increased p53 expression. FACS analysis and assessment of expressions of cell cycle markers revealed HBx induced a release from G1/S arrest in HepG2 cells. Further, cell proliferation assay showed HBx promoted proliferation of HepG2 cell. CONCLUSION: Our study revealed that HBx induced down regulation of miR-122 expression that consequently increased CCNG1 expression. This subsequently caused cell proliferation and release from G1/S arrest in malignant hepatocytes. The study provides the potential to utilize the HBx-miR-122 interaction as a therapeutic target to limit the development of HBV related HCC.

Insights into human immunodeficiency virus-hepatitis B virus co-infection in India.

Shared routes of transmission lead to frequent human immunodeficiency virus (HIV)-hepatitis B virus (HBV) co-infection in a host which results in about 10% of HIV positive individuals to have chronic hepatitis B infection worldwide. In post-antiretroviral therapy era, liver diseases have emerged as the leading cause of morbidity and mortality in HIV-infected individuals and HBV co-infection have become the major health issue among this population particularly from the regions with endemic HBV infection. In setting of HIV-HBV co-infection, HIV significantly impacts the natural history of HBV infection, its disease profile and the treatment outcome in negative manner. Moreover, the epidemiological pattern of HBV infection and the diversity in HBV genome (genotypic and phenotypic) are also varied in HIV co-infected subjects as compared to HBV mono-infected individuals. Several reports on the abovementioned issues are available from developed parts of the world as well as from sub-Saharan African countries. In contrast, most of these research areas remained unexplored in India despite having considerable burden of HIV and HBV infections. This review discusses present knowledge from the studies on HIV-HBV co-infection in India and relevant reports from different parts of the world. Issues needed for the future research relevant to HIV-HBV co-infection in India are also highlighted here, including a call for further investigations on this field of study.