GB virus C/hepatitis G virus infection in KwaZulu Natal, South Africa

Sathar, Mahomed A.; Soni, Paresh N.; Naicker, Saraladevi; Conradie, J. D.; Lockhat, Fathima; Gouws, Eleanor

doi:10.1002/(sici)1096-9071(199909)59:1<38::aid-jmv7>3.0.co;2-3

Cited by 25 publications

(28 citation statements)

References 42 publications

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“…1999a). Phylogenetic analysis of the E2 gene segment from certain KZN isolates is consistent with previous analysis of the 5′ NCR(Sathar et al . 1999a; Smith et al .…”

Section: Phylogenetic Analysis Of Gbv‐c/hgvsupporting

confidence: 88%

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GB Virus C/Hepatitis G Virus (GBV‐C/HGV): still looking for a disease

Sathar

Soni²,

York

2000

Int J Experimental Path

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GB Virus C and Hepatitis G Virus (GBV-C/HGV) are positive, single-stranded flaviviruses. GBV-C and HGV are independent isolates of the same virus. Transmission via the blood-borne route is the commonest mode, although vertical and sexual transmission is well documented. GBV-C/HGV is distributed globally; its prevalence in the general population is 10 fold higher in African countries than in non-African countries. High prevalences of GBV-C/HGV have been found in subjects with frequent parenteral exposure and in groups at high risk of exposure to blood and blood products. The clinical significance of human infection with GBV-C/HGV is currently unclear. The virus can establish both acute and chronic infection and appears to be sensitive to interferon. Only some 12-15% of chronic Non-A, B, C hepatitis cases are infected with GBV-C/HGV. A direct association with liver pathology is still lacking and it is not yet clear as to whether GBV-C/HGV is indeed a hepatotropic virus. Current evidence suggests that the spectrum of association of GBV-C/HGV infection with extrahepatic diseases ranges from haematalogical diseases, aplastic anaemia, human immunodeficiency virus (HIV)-positive idiopathic thrombocytopenia and thalassemia, through to common variable immune deficiency and cryoglobunemia.

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“…1999a). Phylogenetic analysis of the E2 gene segment from certain KZN isolates is consistent with previous analysis of the 5′ NCR(Sathar et al . 1999a; Smith et al .…”

Section: Phylogenetic Analysis Of Gbv‐c/hgvsupporting

confidence: 88%

“…2000). Recently, a new variant of GBV‐C/HGV whose sequences of the 5′ NCR were different from all other known GBV‐C/HGV sequences was identified in the province of KwaZulu Natal (KZN), South Africa (Sathar et al . 1999a).…”

Section: Phylogenetic Analysis Of Gbv‐c/hgvmentioning

confidence: 99%

GB Virus C/Hepatitis G Virus (GBV‐C/HGV): still looking for a disease

Sathar

Soni²,

York

2000

Int J Experimental Path

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“…The prevalence of HGV antibody in different sex was found 3.2% (5/156) in males and 3.1% (3/96) in females. 15 It has been reported that 60%-70% patients develop antibodies after infection. 16 As such, the detection of HGV RNA and anti-E2 is necessary to accurately define the controls was 1 to 5 %, in thalassaemic children 32.6%, asymptomatic carriers of anti-HCV 20.4%, IDUs 18.2%, aplastic anaemia patient 14.3%, CSWs 10% and in chronic liver disease 10% 10. Diagnosis of HGV infection is usually carried out by testing serum for the viral genome and /or antiviral antibody.…”

Section: Resultmentioning

confidence: 99%

“…Prevalence of antibody to HGV in hemodialysis patients in Japan was reported as 7.8% 22 -10.7% 23 and 25.7% from South Africa 15 . Low prevalence of hepatitis G virus antibody in hemodialysis patients may be due to following reasons i) immunocompetent individuals develop antibody at a much higher ratio than immunodepressed patients 17 , ii) HGV infection may be more likely to persist in hemodialysis patients and seroconversion to anti E2 may be less likely to occur 24 and iii) it was also been suggested that seropositivity for anti E2 may be short lasting after seroconversion among hemodialysis patients.…”

Section: Methodsmentioning

confidence: 99%

Low Prevalence of Antibody to Hepatitis G Virus Among the Risk Groups and Healthy Population of Bangladesh

Siddiqua¹,

Nawsher²,

Tabassum

et al. 2012

Bangladesh J Med Microbiol

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Dr Mahmuda Siddiqua E-mail : mahmuda99@yahoo.com hepatitis, occurring in patients with no other known etiology. 5It is well established that HGV maintains a high and stable level of plasma viremia for many years, 6 which indicates it's efficient and active replication. Before the establishment of antibody detection methods, prevalence rates of HGV RNA in general population varied between less than 1 to 4% in different countries.7 With the development of new tests for detection of anti-HGV antibodies about 3 to 20 % of healthy people are found to have antibodies, indicating that the virus is more widely spread worldwide. In particular, rates of HGV seropositivity have ranged between 2-8% in Asia and North America, between 10-15 % in Europe and around 20% in South Africa and South America.

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“…Epidemiological investigations demonstrated that GBV-C/HGV RNA prevalence among blood donors ranges from 0.5-4% in the USA, Europe and Japan (Orito et al 1996, Gutierrez et al 1997, Nübling et al 1997, Blair et al 1998, Sauleda et al 1999) to 10-18.9% in some African countries (Casteling et al 1998, El-Zayadi et al 1999, Sathar et al 1999. In South America, it has also been reported at a varying range from 5.5% in Argentina (Oubiña et al 1999) to 14.6% in Bolivia (Konomi et al 1999).…”

Section: Discussionmentioning

confidence: 99%