29 research outputs found

    Human Bocavirus in Hospitalized Children, South Africa

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    Hepatitis C - a South African perspective

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    The existence of non-A, non-B (NANB) hepatitis was established in the 1970s, when accurate serological tests allowed exclusion of hepatitis A and B viruses as the cause of most cases of post-transfusion hepatitis. The term 'hepatitis C' was coined after molecular cloning of nucleic acid from highly infectious sera of chimpanzees identified an RNA virus as the primary cause of post-transfusion hepatitis (PTH). Sequence analysis and expression of the RNA has shown it to be closely related to the flavi- and pestiviruses. It has marked genomic variability which may affect its biological and immunological characteristics, is transmitted parenterally and sporadically, by as yet unidentified routes, and causes chronic indolent liver disease in 50 - 75% of infected patients. It is associated with hepatocellular carcinoma, glomerulonephritis, cryoglobulinaemia, auto-immune liver disease, lymphocytic sialadenitis and porphyria cutanea tarda. Up to 500 million people worldwide may be infected with hepatitis C virus (HCV), and many questions about the disease remain unanswered. Therapy is still largely ineffective and our current understanding of the long-term natural history, our methods of diagnosis, therapy, prevention and immunisation are suboptimal

    High prevalence of TT virus in a rural community of South Africa

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    To the Editor: The development of new molecular techniques in recent years has resulted in the discovery of a number of novel viruses. Hepatitis C virus (HCV) was the first to be discovered in 1989 using immunoscreening methods 1 and since 1995 a further five new viruses have been identified using the same or modified technologies: GB virus-C/hepatitis G virus (GBV-C/HGV), 2,3 human herpesvirus 8 (HHV8),4 TT virus (TTV),5 SEN virus (SEN-V)6 and human metapneumovirus.7 In each case the prevalence of the virus in different communities, its association with disease and therefore its relevance in the hospital and blood transfusion settings needed to be established

    Molecular Characterization of the 16S rRNA Gene of Helicobacter fennelliae Isolated from Stools and Blood Cultures from Paediatric Patients in South Africa

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    Forty strains of H. fennelliae collected from paediatric blood and stool samples over an 18 year period at a children's hospital in Cape Town, South Africa, were amplified by PCR of the 16S rRNA. Two distinct genotypes of H. fennelliae were identified based on the phylogenetic analysis. This was confirmed by sequencing a portion of the beta subunit of the RNA polymerase (rpoB) gene. All isolates from South Africa clustered with a proposed novel Helicobacter strain (accession number AF237612) isolated in Australia, while three H. fennelliae type strains from the northern hemisphere, NCTC 11612, LMG 7546 and CCUG 18820, formed a separate branch. A large (355bp) highly conserved intervening sequence (IVS) in the 16S rRNA was found in all isolates. Predicted secondary structures of the IVS from the 16S rRNA and 23S rRNA were characterised by a primary stem structure formed by base pairing of the 3′ and 5′ ends and internal loops and stems. This phylogenetic analysis is the largest undertaken of H. fennelliae. The South African H. fennelliae isolates are closely related to an Australian isolate previously reported to be a possible novel species of Helicobacter. This study suggests that the latter is strain of H. fennelliae

    Molecular characterisation of virus in the brains of patients with measles inclusion body encephalitis (MIBE)

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    BACKGROUND: During 2009/10 a major measles epidemic caused by genotype B3 occurred in South Africa. Measles inclusion body encephalitis (MIBE) was diagnosed in a number of highly immuno-compromised HIV patients. The diagnosis was based on typical clinical and MRI findings and positive measles virus PCR in brain or CSF.To characterize the brain virus, nucleoprotein, matrix, fusion and haemagglutinin genes from 4 cases was compared with virus from acutely infected patients. METHODS: cDNA was synthesized using random primers and viral genes were amplified by nested RT-PCR. PCR products were sequenced in the forward and reverse direction and a contig of each gene was created. Sequences were aligned with reference sequences from GenBank and other local sequences. RESULTS: Brain virus was very similar to the South African epidemic virus. Features characteristic of persistent measles virus in the brain were absent. Mutation frequency in brain virus was similar to epidemic virus and had the same substitution preference (U to C and C to U). The virus of 2 patients had the same L454W mutation in the fusion protein. CONCLUSION: The brain virus was very similar to the epidemic strain. The relatively few mutations probably reflect the short time from infection to brain disease in these highly immuno-compromised patients

    Isotachophoresis of human cerebrospinal fluid

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    Human Parainfluenza Virus (HPIV) Detection in Hospitalized Children with Acute Respiratory Tract Infection in the Western Cape, South Africa during 2014–2022 Reveals a Shift in Dominance of HPIV 3 and 4 Infections

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    The epidemiology of human parainfluenza viruses (HPIV), particularly its role as a cause of acute respiratory infection (ARI) in infants, has not been formally studied in South Africa. We evaluated HPIV prevalence in diagnostic samples from hospitalized children from public sector hospitals in the Western Cape between 2014 and 2022. HPIV infection was detected in 2–10% of patients, with the majority of infections detected in children less than 1 year of age. Prior to 2020, HPIV 4 (40%) and HPIV 3 (34%) were the most prevalent types, with seasonal peaks in late winter/spring for HPIV 3 and autumn/winter for HPIV 4. HPIV 4A and 4B co-circulated during the seasonal activity between 2014 and 2017. Pandemic restrictions in 2020 had a profound effect on HPIV circulation and the rebound was dominated by waves of HPIV 3, accounting for 66% of detections and a sustained decline in the circulation of HPIV 1, 2 and 4. An immunity gap could account for the surge in HPIV 3 infections, but the decline in prior HPIV 4 dominance is unexplained and requires further study
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