Global Distribution of Human Protoparvoviruses.

Development of next-generation sequencing and metagenomics has revolutionized detection of novel viruses. Among these viruses are 3 human protoparvoviruses: bufavirus, tusavirus, and cutavirus. These viruses have been detected in feces of children with diarrhea. In addition, cutavirus has been detected in skin biopsy specimens of cutaneous T-cell lymphoma patients in France and in 1 melanoma patient in Denmark. We studied seroprevalences of IgG against bufavirus, tusavirus, and cutavirus in various populations (n = 840), and found a striking geographic difference in prevalence of bufavirus IgG. Although prevalence was low in adult populations in Finland (1.9%) and the United States (3.6%), bufavirus IgG was highly prevalent in populations in Iraq (84.8%), Iran (56.1%), and Kenya (72.3%). Conversely, cutavirus IgG showed evenly low prevalences (0%-5.6%) in all cohorts, and tusavirus IgG was not detected. These results provide new insights on the global distribution and endemic areas of protoparvoviruses.

Molecular detection and phylogenetic analysis of Kenyan human bocavirus isolates.

INTRODUCTION: The commonly expected causative agents associated with flu-like symptoms in Kenya are the classical viral pathogens identifiable as influenza virus, adenovirus, parainfluenza virus, enteroviruses, respiratory syncytial virus (RSV) and rhinovirus. However, newer agents have been identified globally that present with illnesses clinically indistinguishable from those caused by the classical pathogens; one of them is human bocavirus. METHODOLOGY: A total of 384 specimens were analyzed, primarily to determine if the emerging human bocavirus (HBoV) infections exist in Kenya as coinfections with other respiratory viruses and to describe the genotype of the virus in circulation. In brief, viral nucleic acids were extracted from culture supernatants, amplified by PCR, and sequenced. RESULTS: HBoV DNA was amplified from 1.8% of screened specimens. Coinfection with parainfluenza virus, adenovirus, and enterovirus was 2.5%, 2%, and 1.4%, respectively. Multiple coinfections consisting of HBoV plus two other viruses were found in 3% of specimens. Isolation occurred in the months of January, March, April, August, and November. Retrospective review of clinical parameters indicated that all the individuals complained of non-specific symptoms, mainly fever, coughs, nasal stuffiness, runny noses, and vomiting. Phylogenetically, the GenBank deposited sequences of this study's isolates cluster closely to the reference strain NC_07455 (HBoV1). CONCLUSION: Coinfections with human bocavirus (HBoV1) occur in Kenya, and high incidence might primarily be during the early stages of children's lives.

Enhanced discrimination of African swine fever virus isolates through nucleotide sequencing of the p54, p72, and pB602L (CVR) genes.

Complete sequencing of p54-gene from 67 European, American, and West and East African Swine Fever virus (ASFV) isolates revealed that West African and European ASFV isolates classified within the predominant Genotype I according to partial sequencing of p72 were discriminated into four major sub-types on the basis of their p54 sequences. This highlighted the value of p54 gene sequencing as an additional, intermediate-resolution, molecular epidemiological tool for typing of ASFV viruses. We further evaluated p54-based genotyping, in combination with partial sequences of two other genes, for determining the genetic relationships and origin of viruses responsible for disease outbreaks in Kenya. Animals from Western and central Kenya were confirmed as being infected with ASFV using a p72 gene-based PCR assay, following outbreaks of severe hemorrhagic disease in domestic pigs in 2006 and 2007. Eleven hemadsorbing viruses were isolated in macrophage culture and genotyped using a combination of full-length p54-gene sequencing, partial p72-gene sequencing, and analysis of tetrameric amino acid repeat regions within the variable region of the B602L gene (CVR). The data revealed that these isolates were identical in their p72 and p54 sequence to viruses responsible for ASF outbreaks in Uganda in 2003. There was a minor difference in the number of tetrameric repeats within the B602L sequence of the Kenyan isolates that caused the second Kenyan outbreak in 2007. A practical implication of the genetic similarity of the Kenyan and Ugandan viral isolates is that ASF control requires a regional approach.