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Diverse genotypes of Kaposi's sarcoma associated herpesvirus (KSHV) identified in infant blood infections in African childhood-KS and HIV/AIDS endemic region.

Kasolo FC, Spinks J, Bima H, Bates M, Gompels UA - J. Med. Virol. (2007)

Bottom Line: This current enlarged study analyses blood infections of 200 hospitalized infants (6-34 months age) with symptoms of fever as well as upper respiratory tract infection, diarrhoea, rash or rhinitis.KSHV and HIV viraemia and were prevalent in this group, 22% and 39%, respectively.This supports the interpretation that the acquisition of childhood KSHV infections and subsequent development of KS are due to additional co-factors.

View Article: PubMed Central - PubMed

Affiliation: Virology Department, University Teaching Hospital, University of Zambia Medical School, Lusaka, Zambia.

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Coding changes in the K12 Kaposin A gene. Zambian infant blood KSHV K12 B genotypes (from Fig. 3) compared to protein encoded by reference P type genome (GK18) [Rezaee et al., 2006]. A disrupted motif reported required for transformation is underlined [Tomkowicz et al., 2005].
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fig04: Coding changes in the K12 Kaposin A gene. Zambian infant blood KSHV K12 B genotypes (from Fig. 3) compared to protein encoded by reference P type genome (GK18) [Rezaee et al., 2006]. A disrupted motif reported required for transformation is underlined [Tomkowicz et al., 2005].

Mentions: Despite the diversity of genotypes identified in the infant blood KSHV infections, is there any evidence for distinct strains for childhood transmission? The K1A5 genotype is prevalent in KS biopsy samples from patients in regions of Africa where there is childhood endemic KS [Kasolo et al., 1998; Lacoste et al., 2000; Kakoola et al., 2001]. Furthermore, the P genotype of K14.1/15 is also linked to this region [Lacoste et al., 2000], where only one M genotype was identified. Moreover, only the K12 B genotype (both B1 and B2) was identified in these infant infections, and these genotypes are dominant in adult KS identified in other African regions [Poole et al., 1999; Lacoste et al., 2000; Kakoola et al., 2001]. Most of the K12 variation is in the 30 non–coding intergenic region. However, the encoded Kaposin A is a tumorigenic transforming gene interacting with cytohesin–1 integrin regulator, and two coding changes were identified (Fig. 4) [Muralidhar et al., 1998; Kliche et al., 2001]. One shown in some B1 genotypes,C64G gives rise to Leu34 to Val, though conservative, it disrupts an LXXLL motif (to LXXVL), reported required for cellular transformation [Tomkowicz et al., 2005]. The other substitution is divergent, G112C, giving Ala50 to Pro in all B genotypes compared to both referenceMand P type genomes (BC1 and GK18, respectively) [Russo et al., 1996; Rezaee et al., 2006]. Thus several genotype markers may link with childhood endemic KS endemic regions. However, the observation of multiple K1 genotypes and past evidence for linked genome diversity [Poole et al., 1999], suggests multiple KSHV strains can be transmitted to infants.


Diverse genotypes of Kaposi's sarcoma associated herpesvirus (KSHV) identified in infant blood infections in African childhood-KS and HIV/AIDS endemic region.

Kasolo FC, Spinks J, Bima H, Bates M, Gompels UA - J. Med. Virol. (2007)

Coding changes in the K12 Kaposin A gene. Zambian infant blood KSHV K12 B genotypes (from Fig. 3) compared to protein encoded by reference P type genome (GK18) [Rezaee et al., 2006]. A disrupted motif reported required for transformation is underlined [Tomkowicz et al., 2005].
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2683451&req=5

fig04: Coding changes in the K12 Kaposin A gene. Zambian infant blood KSHV K12 B genotypes (from Fig. 3) compared to protein encoded by reference P type genome (GK18) [Rezaee et al., 2006]. A disrupted motif reported required for transformation is underlined [Tomkowicz et al., 2005].
Mentions: Despite the diversity of genotypes identified in the infant blood KSHV infections, is there any evidence for distinct strains for childhood transmission? The K1A5 genotype is prevalent in KS biopsy samples from patients in regions of Africa where there is childhood endemic KS [Kasolo et al., 1998; Lacoste et al., 2000; Kakoola et al., 2001]. Furthermore, the P genotype of K14.1/15 is also linked to this region [Lacoste et al., 2000], where only one M genotype was identified. Moreover, only the K12 B genotype (both B1 and B2) was identified in these infant infections, and these genotypes are dominant in adult KS identified in other African regions [Poole et al., 1999; Lacoste et al., 2000; Kakoola et al., 2001]. Most of the K12 variation is in the 30 non–coding intergenic region. However, the encoded Kaposin A is a tumorigenic transforming gene interacting with cytohesin–1 integrin regulator, and two coding changes were identified (Fig. 4) [Muralidhar et al., 1998; Kliche et al., 2001]. One shown in some B1 genotypes,C64G gives rise to Leu34 to Val, though conservative, it disrupts an LXXLL motif (to LXXVL), reported required for cellular transformation [Tomkowicz et al., 2005]. The other substitution is divergent, G112C, giving Ala50 to Pro in all B genotypes compared to both referenceMand P type genomes (BC1 and GK18, respectively) [Russo et al., 1996; Rezaee et al., 2006]. Thus several genotype markers may link with childhood endemic KS endemic regions. However, the observation of multiple K1 genotypes and past evidence for linked genome diversity [Poole et al., 1999], suggests multiple KSHV strains can be transmitted to infants.

Bottom Line: This current enlarged study analyses blood infections of 200 hospitalized infants (6-34 months age) with symptoms of fever as well as upper respiratory tract infection, diarrhoea, rash or rhinitis.KSHV and HIV viraemia and were prevalent in this group, 22% and 39%, respectively.This supports the interpretation that the acquisition of childhood KSHV infections and subsequent development of KS are due to additional co-factors.

View Article: PubMed Central - PubMed

Affiliation: Virology Department, University Teaching Hospital, University of Zambia Medical School, Lusaka, Zambia.

Show MeSH
Related in: MedlinePlus