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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative organism for Coronavirus Disease 2019 (COVID-19), originated in Wuhan, China and has now spread to most parts of the world. A pandemic of this magnitude has not been witnessed in more than 100 years since the Spanish flu in 1918. The major challenge for scientists and doctors worldwide has been to find a therapeutic intervention to prevent the spread and development of this disease. As more research is being done, the pathophysiology of COVID-19 has been explained, although no effective therapy has been found. Multiple drugs and therapies are under trials and a few have shown inconclusive results. The attempts have ranged from repurposing drugs to trying to develop new vaccines. Formulation of guidelines pose another challenge to the government and international agencies owing to the lack of data. These agencies have constantly released and updated guidelines based on new research and growing knowledge. In this review, we aim to compare and bring out the different international guidelines for management of COVID-19, along with a review of tried therapeutic interventions and their primitive results. The COVID-19 has been a major global health crisis that is overpowering most heath care systems and multiple agencies and research teams are trying to limit and manage this spread. Currently no effective treatment is available and guidelines differ regarding the drugs that can be used, which are mostly off-label.

Background & objectives: Clinical outcome after hepatitis B virus (HBV) exposure varies extremely from spontaneous clearance to chronic hepatitis B and often progresses to liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Host genetic factor plays an important role in the regulation of immune response. This study was aimed to investigate whether HLA class II DQA1 and DQB1 gene polymorphism were associated with chronic hepatitis B infection and in the development of HBV-related LC and HCC. Methods: DQA1 and DQB1 allele polymorphism were studied in 187 patients with HBV-related liver diseases (which included 73 chronic hepatitis B, 84 LC and 30 HCC patients) and 109 controls who had spontaneously recovered from HBV infection using polymerase chain reaction amplification with sequence-specific primers. Results: Our data suggested that DQA1*0101/2/4 [odds ratio (OR)=2.78; Pc=0.003], DQA1*0103 (OR=2.64; Pc=0.0007) and DQB1*0302/3 (OR=2.15; Pc=0.01) were associated with the protection from chronic HBV infection, whereas DQB1*0402 (OR=0.25; Pc=0.001) showed susceptible effect on chronic HBV infection. DQB1*0601 (OR=3.73; Pc=0.006) conferred protective effect from developing LC; similarly, DQB1*0302/3 (OR=5.53; Pc=0.05) and DQB1*0402 (OR=0.00; Pc=0.001) conferred protective effect from developing HCC. However, DQA1*0601 and DQB1*0503 showed susceptible effect on chronic HBV infection; these associations were no longer significant after Bonferroni correction. Interpretation & conclusions: Our results revealed HLA-DQA1*0101/2/4 - DQA1*0103 - DQB1*0302/3 and DQB1*0601 as protective and DQB1*0402 as risk alleles. The study suggests that various subtypes of HLA-DQA1 and DQB1 are associated with both HBV clearance and development of chronic HBV infections.

Aims: In virus-infected cells, pattern recognition receptors (PRRs) recruits their specific adaptor molecules, mitochondrial antiviral signaling protein (MAVS), TIR-domain-containing adapter-inducing interferon-β (TRIF) and TNF receptor associated factor (TRAF6) which induces interferon. Toll-like receptor 3 (TLR3) induces activation of the NF-kappa B (NF-κB) for interferon production. The study has been designed to assess the correlation of TLR3, MAVS, TRIF and TRAF6 outcome of HCV infection. Methods: The 46 chronic hepatitis C (CHC) patients were screened for LFT (Liver function test), HBsAg, Anti HCV, viral load, histology and expression of TLR3, MAVS, TRIF and TRAF6 genes. Out of 46 CHC patients, 7 were on therapy. The 12 healthy controls were screened for LFT, HBsAg, Anti HCV, gene expressions. The gene expressions were studied in liver tissue and measured using semi-quantitative analysis of Western blots. Results: The expression of TRAF6 was independent of HCV infection. The expression of TRIF, TLR3 and MAVS were significantly (p< 0.05) down regulated in CHC (N = 46) compared to healthy controls (N = 12), in high viral load (N = 21) compared to low viral load (N = 25), in HAI (Histology activity index) 1-4 (N = 12), 5-8 (N = 16), 9-12 (N = 8), 13-18 (N = 5) compared to HAI 0 (N = 5) cases. The significant reduction in the expression of TRIF, TLR3 and MAVS was observed in non-responder (N = 3) compared to responder (N = 4) after treatment (p

nCOVID-19 (2019 novel corona virus) is a naive infective virus that brought the whole world to standstill. The clinical features attributing to its infection have a broad spectrum, ranging from minimally symptomatic to respiratory failure and death. The aim of present case series was to assimilate data regarding the clinical characteristics of first 11 cases of COVID-19 infection in the local population of Andaman and Nicobar Islands. Various clinical features, biochemical and individual parameters were compiled that may affect the disease evolution and then, subjected to descriptive analysis. Out of 11 patients, six patients had a definitive known source of their infection and four patients had history of close contacts with first six ones. Only one patient had unknown source of the infection. Majority of the patients remained asymptomatic to pauci-symptomatic. Mean duration of symptomatic period was less than seven days (5.6 days). In this series, out of 11 patients, 2 (18%) were females and rest all were males (82%). Four of the patients had fever, four had cough and four had weakness and fatigue, two had malaise, three had anorexia, one had dyspepsia and one diarrhea. None of the patient landed in Intensive care unit (ICU). Patients were treated with empirical combination therapy including Azithromycin (500 mg OD) and Oseltamivir (75 mg BD) irrespective of their symptoms. Additionally, Hydroxychloroquine (200 mg BD) was given to symptomatic ones. Conclusively, less dreadful clinical presentation of this infection was faced in this population.

Summary The basis of hepatitis C virus (HCV) evasion of immune system and its response to treatment is still elusive. There have been studies where the level of C4 has been found to be associated with HCV persistence and disease progression. This study aims to find out relationship between levels of C4 in serum, and its functional SNPs with response to treatment. The study included 84 patients with CHC who received treatment and 75 healthy controls. C4 expression, both at mRNA and protein level, was estimated by Real time and ELISA respectively. Its functional SNP's genotyped by AS-PCR. The mean ± SD baseline C4 levels between the disease and healthy cases was significantly different (1075.74 ± 65.25 vs 1593 ± 24.55 ng/mL, P

The basis of response of chronic hepatitis C (CHC) patients to treatment is still unclear, and there may be many other factors which influence treatment outcome other than the existing ones. The serum concentration of C3 closely reflects the total complement activity, and individuals affected by C3 deficiency suffer from recurrent pyogenic infections. This study aims to find out relationship between levels of C3 in serum and its functional SNPs with response to treatment. The study included 132 CHC patients of which 48 received Pegylated IFN+Ribavirin and 81 controls. C3 levels and its three known functional SNP's genotyped by ELISA and SSP PCR, respectively. C3 Level of the healthy group was significantly higher (88.5 ± 19 mg/dL) when compared to CHC group (56 ± 18 mg/dL; P < 0.001). Thirty-three of 36 responders were rs2230201 CC genotype carriers, whereas 9 of 12 nonresponders were non-CC genotype. The 'C' allele of rs2230201 was found to be associated with increased serum C3 levels when compared to other genotypes in healthy group, whereas CT genotype was associated with lowered serum C3 in CHC group. A serum C3 value of

Introduction Chromosomal abnormalities are the results of alterations in the number or structure of chromosomes causing significant human morbidity and mortality. They are responsible for a large proportion of miscarriages, developmental delay, disorders of sexual development, congenital malformations and mental retardation. Aim The aim of this study was to describe the prevalence of different chromosomal abnormalities in North Indian patients referred for cytogenetic analysis. Materials and methods Total of 859 patients ranging from newborn to 37 years of age were referred to the division of genetics, Department of Paediatrics between 2010 and 2015, with a variety of clinical disorders; Down syndrome (DS), Turner's syndrome (TS) and Klinefelter syndrome; amenorrhea; ambiguous sex and multiple congenital malformations. Chromosomal analysis was performed on lymphocyte culture according to standard methods. Results Of the 859 cases studied, 371 (43.1%) had chromosomal abnormalities. The most common autosomal abnormalities were DS 302 (81.4%) and sex chromosomal abnormalities were TS 51 (13.7%). Numerical abnormalities were accounted for 353 (41.0%) and structural abnormalities 18 (2.0%), respectively. Various other chromosomal anomalies were also reported. Conclusion We have reviewed the incidence and distribution of chromosomal abnormalities and found higher rate of chromosomal abnormalities 43.1% in the referred cases. Our data suggest that chromosomal analysis is important tool in the evaluation of genetic disorders and helps clinicians to provide accurate diagnosis and proper genetic counselling.

Background/objective Quantification of serum hepatitis B antigen (HBsAg) is an important test that marks active infection with hepatitis B and helps in the prediction of the clinical outcome and management of hepatitis B virus (HBV) infection. Correlation with HBV DNA quantitative levels may help in developing strategies for antiviral treatment. This study is aimed to evaluate HBsAg titres in various phase of HBV infection in HBsAg positive patients, and its correlation with HBV DNA viral load levels. Methods 976 HBV related patients were analysed in this retrospective cross-sectional study. Patients were categorised on the basis of the phase of HBV infection: immune tolerant phase (IT, n =123), immune clearance phase (IC, n =192), low-replicative phase (LR, n =476), and HBeAg-negative hepatitis (ENH, n =185). HBsAg titres were quantified and correlated with HBV-DNA levels and clinical parameters. Results Median HBsAg titres were different between each phases of HBV infection ( P r =0.694, P r =0.603, P r =0.523, P r =0.362, P r =0.110, P =0.04). No correlation was observed between serum HBsAg levels and biochemical parameters. Conclusion The study demonstrated significant difference in the median baseline values of serum HBsAg titres in different phases of HBV infection and provides additional information in understanding the natural history of HBV-infection.

Background and aim Progression of hepatitis B virus infection (HBV) might be affected by host genetic factors. The present study was undertaken to study the role of glutathione S-transferases (GST)-M1 and T1 gene polymorphisms in different stages of HBV infection: HBV inactive carrier, chronic hepatitis B and cirrhosis, and cryptogenic cirrhosis. Methods The study population comprised of 170 subjects; 120 cases (HBV inactive carrier, n =30; HBV related chronic hepatitis, n =30; HBV related cirrhosis, n =30; cryptogenic cirrhosis, n =30) and 50 unrelated healthy adults without liver disease as controls. Analysis of GSTM1 and GSTT1 gene polymorphisms was done by multiplex polymerase chain reaction. Results The GSTM1 null genotype was seen more commonly in hepatitis B cirrhosis ( n =21; 70%), chronic hepatitis B ( n =19; 63.33%) and cryptogenic cirrhosis ( n =17; 56.67%) as compared with inactive carrier ( n =9; 30%) and controls ( n =13; 26%). The GSTT1 null genotype was seen less frequently in all the groups, the observed frequencies were controls ( n =7; 14%), inactive carrier ( n =5; 16.67%), chronic hepatitis B ( n =8; 26.67%) and hepatitis B cirrhosis ( n =7; 23.33%). The difference of GSTM1 null genotype frequencies was statistically significant for hepatitis B cirrhosis vs. controls ( P =0.0002), chronic hepatitis B vs. controls ( P =0.002) and cryptogenic cirrhosis vs. controls ( P =0.01). The GSTT1 null genotype was not found to vary significantly between the groups. Conclusion The patients with GSTM1 null genotype are at risk of progression of liver disease as the frequency of GSTM1 null genotype was found to be significantly higher in chronic hepatitis B, hepatitis B cirrhosis and cryptogenic cirrhosis as compared with controls.

Interleukine-18 (IL-18) was originally called interferon (INF-γ) inducing factor and plays a critical dual role in Th1 polarization and viral clearance. We aimed to explore whether single-nucleotide promoter polymorphisms (SNPs) are associated with the outcome of hepatitis B virus (HBV) infection. 271 HBV infected patients were recruited in this study out of these 109 were spontaneously recovered and 162 were diagnosed to be having persistent HBV infection which includes 48 chronic hepatitis, 84 liver cirrhosis, 30 HCC cases and were compared with 280 healthy controls. IL-18 promoter genotyping was performed with sequence-specific primers. The results demonstrated the significant involvement of genotype AA at position -607 in healthy controls (38.6%) when compared to cases (26.0%) (OR = 0.54 (0.385–0.797)) and also associated with spontaneous clearance (37.6%) compared to persistent HBV infections (17.9%) (OR = 2.76 (1.582–4.832)). Whereas, genotype CC at position -607 in cases (18.0%) when compared to healthy controls (6.7%) (OR = 3.03 (1.734–5.303)) also associated with persistent HBV infections (24.1%) compared to spontaneous clearance (9.2%) (OR = 0.31 (0.151–0.67)). And genotype GC at position -137 in cases (49.5%) compared to healthy controls (38.5%) (OR = 1.55 (1.11–2.18)). Whereas, genotype GG at position -137 in healthy controls (56.8%) compared to cases (45.4%) (OR = 0.63 (0.451–0.885)). No significant difference at position -137 was observed between spontaneous clearance and persistent HBV infections. These polymorphisms of the IL-18 gene promoter region at position -607 and -137 could be associated with different outcomes of HBV infection. The people with allele A at position -607 may be protected against HBV infection; moreover AA genotype is associated with spontaneous clearance.

Background: Interleukin-18 (IL-18) is a pro inflammatory cytokine which plays a key role in the acute and chronic inflammatory phases of Rheumatoid Arthritis (RA). The Single Nucleotide Polymorphisms (SNPs) of IL-18 gene promoter region at positions -137 and -607, are postulated to be associated with RA. To test this, this study aimed to identify the association between these SNPs of the IL-18 gene promoter region of RA in south Indian patients. Materials and Methods: This study was carried on 190 subjects among which 90 were RA patients and 100 were age and sex matched controls. Genomic DNA was extracted by Salting out method. IL 18 gene promotor region SNPs, IL 18 - 607 and IL 18 -137 were amplified by using sequence specific primers. The amplified products of different samples were separated by using a 1.5% agarose gel, stained with ethidium bromide and photographed. All statistical analyses were carried out by using SYSTAT 12 software. Results: At position 607, the frequencies of C allele, CC genotype, A allele and AA genotype were found to be significantly higher in patients and controls respectively and there was no significant difference in CA genotype. At position 137, there was no significant difference between the two groups with regard to G and C allelles but there was a significant increase in GG genotype of patients and CC genotype of controls. There was no association between duration of morning stiffness, rheumatoid factor positivity or negativity, age of onset and gender with distribution of genotypes and alleles. Conclusion: C allele, CC genotype at position-607 and GG genotype at position-137 are risk factors and A allele, AA genotype at position-607 and CC genotype at position-137 have protective effect for RA.

Hepatitis E has both a high incidence and severe course in pregnant women in some geographic regions of HEV (Hepatitis E virus) endemic countries. Intrauterine fetal death, preterm delivery, and perinatal mortality are reported to be higher in pregnant women with HEV infection. Alteration in the steroid hormone levels show high incidence of FHF (Fulminant Hepatic Failure) with high mortality in hepatitis E during pregnancy. The present study is designed to look for the association between ESR (Estrogen Receptor)-beta gene polymorphism for Alu I restriction site and pregnancy outcome. The study group comprised of 142 pregnant women with HEV infection in third trimester, 103 AVH (Acute Viral Hepatitis) cases and 39 ALF (Acute Liver Failure) cases. The control group comprised of 142, age and gestation matched healthy pregnant women with no obstetrics and medical complications. The inclusion criteria for the study group are pregnant women in third trimester with positivity to HEV IgM and/or HEV RNA in the age group of 18-40 years. Genomic DNA is extracted from peripheral blood leukocytes using DNA extraction kit according to the manufacturer’s instructions. The polymorphism study is done by using ESR2 specific primers and its genotype is determined by Alu I restriction enzyme. The occurrence of variant A allele for AluI restriction site is significantly higher in mothers with HEV infection who had preterm (25%) than full term delivery (10%) with OR 2.989 (95% CI = 1.265-8.084, p