Dengue in India.

Dengue virus belongs to family Flaviviridae, having four serotypes that spread by the bite of infected Aedes mosquitoes. It causes a wide spectrum of illness from mild asymptomatic illness to severe fatal dengue haemorrhagic fever/dengue shock syndrome (DHF/DSS). Approximately 2.5 billion people live in dengue-risk regions with about 100 million new cases each year worldwide. The cumulative dengue diseases burden has attained an unprecedented proportion in recent times with sharp increase in the size of human population at risk. Dengue disease presents highly complex pathophysiological, economic and ecologic problems. In India, the first epidemic of clinical dengue-like illness was recorded in Madras (now Chennai) in 1780 and the first virologically proved epidemic of dengue fever (DF) occurred in Calcutta (now Kolkata) and Eastern Coast of India in 1963-1964. During the last 50 years a large number of physicians have treated and described dengue disease in India, but the scientific studies addressing various problems of dengue disease have been carried out at limited number of centres. Achievements of Indian scientists are considerable; however, a lot remain to be achieved for creating an impact. This paper briefly reviews the extent of work done by various groups of scientists in this country.

Tick-borne pathogens and diseases of animals and humans in Thailand.

Tick-borne pathogens in Thailand can cause diseases that result in productivity and economic losses in the livestock sector as well as cause debilitating illnesses in humans and their companion animals. With the advent of molecular techniques, accurate identification of tick-borne pathogens and precise diagnosis of disease is now available. This literature review summarizes the various tick-borne pathogens that have been isolated from ticks and their vertebrate hosts in Thailand, covering those protozoa, rickettsiae, bacteria and viruses most responsible for human and veterinary disease with particular emphasis on those that have been characterized molecularly.

Evaluation of HGV viremia prevalence and its co- infection with HBV, HCV, HIV and HTLV-1 in hemophilic patients of Southern Khorassan, Iran

The GB virus-C [GBV-C] and Hepatitis G virus [HGV], collectively known as GBV-C/HGV and transmitted through blood transfusion and blood components. A co-infection of HGV and HCV is often seen in patients with hemophilia. The paucity of information about rate of GBV-C infection among hemophilic patients in Iran promoted the current study. This study was performed on 80 hemophilic patients from south Khorassan branch of Iranian hemophilia society in Birjand. All 80 serum samples were tested for hepatitis B surface antigen [HBs-Ag], Anti HCV, Anti HIV, and Anti HTLV-1. All sera positive for HCVAb were retested by recombinant immunoblot assay as a complementary test. Also, Serum HCV-RNA, HCV genotyping and HGV-RNA were detected. The prevalence of HGV-RNA was 5% [4 of 80]. The prevalence of Anti HCV positive was 26.3% [21 of 80] and HCV- RNA was detected in 80% [17 of 21] of these patients. Co infection of HGV with HCV was 5%. HBsAg and Anti HIV were negative in all of our patients. Anti HTLV-1 was detected in one patient [1.25%]. HGV and HCV are prevalent in South Khorassan hemophilic patients. Prevalence of HGV infection is less than HCV but it is more prevalent than HBV, HIV and HTLV-1 infection

Hepatitis G virus (HGV): current perspectives.

Five viruses are usually associated with hepatitis in humans: A-E. In addition to these viruses as aetiological agents of hepatitis, there remain a number of patients with hepatitis in whom no virus could be identified. It was therefore postulated that there may be other agents which may be causing hepatitis. Recently, two viruses have been associated with hepatitis: hepatitis G virus (HGV), and transfusion transmissible virus (TTV). Hepatitis G virus (HGV) is a single stranded RNA virus which represents a newly discovered virus belonging to the flavivirus family. HGV is distinct from hepatitis C virus (HCV) and the newly discovered GBV-A and GBV-B agents, while GBV-C represents an isolate of HGV. The structure of the HGV genome resembles that of HCV. HGV replicates in peripheral blood cells, while replication in liver cells has not been observed till date. Diagnosis of HGV infection is mainly by use of polymerase chain reaction (PCR), as serological techniques are still being developed. Epidemiological data indicate that the virus is prevalent throughout the world, including India and is transmitted via blood/blood products, sexually and vertically from infected mothers to children. The relationship between infection with the virus and presence of liver pathology is controversial and has not been proven beyond doubt, as majority of patients with HGV have no detectable evidence of disease.

Prevalencia de infección por virus de hepatitis G en una cohorte de pacientes hemofílicos HIV+ / [Prevalence of hepatitis G virus infection in a cohort of hemophilic HIV positive patients]

We analysed the prevalence of hepatitis G virus (HGV) infection in HCV+/HIV+ hemophilic patients determining HGV viremia in plasma by polymerase chain reaction (PCR). The overall prevalence of HGV infection was 13.51

. Viremia by HGV was more frequent in younger patients. Two subgroups of patients were considered taking into account prognosis of HIV disease progression. The prevalence of HGV infection was significantly higher in those with better prognosis and low risk of evolution to AIDS. The results suggest that HGV infection may slow disease progression, directly or indirectly.