Clinical profile, genotype and management updates of hepatitis B virus.

Hepatitis B virus (HBV) is a well known agent of acute and chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. Around 400 million people worldwide carrier of HBV of which more than 250 million reside in Asia, and 1-2 million people have died from it. It has a partially double-stranded DNA, having 3.2-kb genome size and replicate via reverse transcription of RNA intermediate. In the natural history or during the antiviral therapy of chronic HBV infection, seroconversion from HBeAg to anti-HBeAg is usually accompanied by a decrease in viral replication and remission of liver disease. Based on genomic sequence data HBV is classified into eight genotypes A-H and four major serotypes ayw, ayr, adw and adr on the basis of complete genome and S gene sequence analysis. Genotypes and serotypes are useful tools in understanding the epidemiology of HBV infection. HBV genotypes have distinct geographical distributions. The HBV variants appear during HBeAg seroconversion and they bring mutations in the precore region (PC) that prevent HBeAg synthesis. Another common HBeAg variant is the basal core promoter mutant (BCP) characterized by point mutation in the promoter of both HBeAg mRNA and core protein mRNA. The most frequent core promoter mutation is the double A1762T and G1764A nucleotide exchange, which results in a substantial decrease in HBeAg expression but enhanced viral genome replication. The approved antiviral drugs such as Interferon, lamivudine, adefovir dipivoxil, entecavir and telbivudine for purpose of treating chronic HBV infection is to prevent or stop the progression of liver injury by suppressing viral replication or eliminating infection. Sustained losses of viral markers of active viral replication (HBeAg and HBV DNA) are the standard end point of the therapies.

Distribution of hepatitis B virus genotypes and its association with severity of liver disease in patients with chronic hepatitis B in uttar pradesh, India.

The present study was designed to investigate the distribution of genotypes and its association with severity of liver disease in patients with Chronic Hepatitis B (CHB) in Uttar Pradesh, India. One hundred five HBsAg positive patients were selected for the study. The DNA was extracted by using pure viral DNA extraction kit. The genotype of Hepatitis B virus (HBV) was identified by using polymerase chain reaction- based restriction fragment length polymorphism (PCR-RFLP) method, by using AvaII and DpnII restriction enzyme to see the different patterns of cleavage that would occur at this specific site. Among 105 HBsAg positive chronic liver disease patients 58 patients were positive for HBeAg and 47 samples were HBeAg negative. Genotyping was done successfully in 91 samples. Genotype A was identified in 22% and genotype D in 78% CHB patients. Genotype A showed elevated liver enzymes much more than genotype D. The Child Pugh classification of 20 patients with genotype A was class A (n = 2), B (n = 9), C (n = 9) and of genotype D was class A (n = 13), B (n = 50) and C (n = 8). In conclusion our results showed that Genotype D was the commonest genotype in Uttar Pradesh, whereas genotype A had significantly more elevated ALT/AST levels than genotype D. (P < 0.05). Child Pugh Grade B was significantly more in patients with genotype D, whereas Child Pugh Grade C was more in genotype A.

Helicobacter pylori and gastric cancer.

Helicobacter pylori has been the subject of intense investigation since its culture from a gastric biopsy in 1982. From the beginning, this gram-negative bacterium has provoked the interest of bacteriologists, gastroenterologists, infectious disease specialists, cancer biologists, epidemiologists, pathologists, and pharmaceutical scientists. Pathologists were among the first groups of scientists to reevaluate their data in the context of the newly discovered bacterial etiological agent. Chronic inflammation elicited by the bacterium provided the missing link in the progression to gastric carcinoma; accordingly, H. pylori was named as a class 1 carcinogen by the World Health Organization. Two key papers published in 1991 in the Journal of the National Cancer Institute reported a positive association between gastric cancer and H. pylori infection. This fact provided a strong rationale to treat all who tested positive for H. pylori. Antibiotic regimens have been largely successful, but some agents such as metronidazole and clarithromycin have been rendered ineffective in several countries and geographical areas of the United States by the emergence of strains resistant to these compounds. Although there was some skepticism initially, within few years numerous research groups verified the association of H.pylori with gastric carcinoma. Host related factors for the development of disease can indicate genetic susceptibility (or resistance) or acquired influences, which may stimulate defenses of the host against environmental carcinogens like H.pylori. The present article is a mini-review of the history and epidemiology of the bacterium and its suggested association with the development and progression of gastric cancer.

Identification of a hepatitis B virus core promoter mutant by PCR- RFLP in patients suffering from chronic liver disease, Uttar Pradesh, India.

OBJECTIVE: The present study was designed to identify a core promotor mutation in the HBV genome in patients suffering from HBV related chronic liver disease. MATERIALS AND METHODS: 154 chronic liver disease patients were selected for study of DNA extracted using a pure viral DNA extraction kit. The core promoter mutation was detected by the polymerase chain reaction- based restriction fragment length polymorphism (PCR-RFLP) method, using the Sau 3AI restriction enzyme to see if cleavage would occur at this specific site. RESULTS: Among the total of 154, 78 patients were found positive for HBsAg and 71 samples were found to be positive for HBV DNA by first round PCR. The over all prevalence of core mutant was 51(71%) in the 71 patients. 11 (68.8%) of 16 patients, excluding 1 patients with mixed type mutation was detected in inactive HBsAg carriers, 39 (81.3%), excluding 2 patients with mixed type was detected in chronic hepatitis B, and 4/7 (57%) in patients with liver cirrhosis were found. CONCLUSION: Our study concluded that the prevalence of the core promoter mutation in the BCP region was higher in the patients with chronic hepatitis B than in liver cirrhosis and HBsAg carriers. The Sau3AI assay, which is much more convenient than sequencing, was shown to be useful for the detection of the core promoter mutant in an extensive number of clinical samples. Monitoring and detection of HBV variants by PCR-RFLP in chronic infection may improve the management of these patients.