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  • Autor: Rajiv T. Erasmus x
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Mini review article. Human herpesvirus-6 and the etiology of multiple sclerosis: a literature review


Background: There is no consensus in the literature on the role of human herpes virus-6 (HHV-6) in multiple sclerosis (MS) onset or progression.

Objective: We evaluated a possible role for HHV-6 in MS onset and progression.

Methods: We conducted a literature search of PubMed and Google scholar with the following search terms: (“multiple sclerosis” OR “MS”) and (“Human Herpes Virus-6” OR “HHV-6”).

Results: A total 21 publications were retrieved, of which 19 case-control studies were included. A further 25 articles were retrieved for background information.

Conclusion: There was insufficient evidence to support a role of HHV-6 in MS onset and progression.

Open access
High Molecular Weight Adiponectin Levels are Neither Influenced by Adiponectin Polymorphisms Nor Associated with Insulin Resistance in Mixed-Ancestry Hyperglycemic Subjects from South Africa


Background: High molecular weight (HMW) adiponectin has antiatherogenic, antiinflammatory and antidiabetic properties and these effects have been linked to its effect on high density lipoprotein cholesterol (HDL-c). Single nucleotide polymorphisms (SNPs) in the adiponectin gene influence adiponectin levels. We examined the relationship between HMW-adiponectin levels and cardiometabolic traits in normo- and hyperglycemic mixed ancestry South Africans and correlated these levels to two common polymorphisms.

Methods: HMW-adiponectin was determined in 101 subjects from the Cape Town Bellville South community-based study on a mixed ancestry population. Comparisons were made between individuals with normo- and hyperglycemia. Two common SNPs, ADIPOQ SNPs rs17300539 and rs266729, known to affect adiponectin levels were also tested for. Levels of HMW-adiponectin were then correlated with cardiometabolic traits in all groups.

Results: Levels of HMW-adiponectin were not significantly different in the normo- and hyperglycemic groups (median 11.6 vs. 10.5 μg/mL, p=0.3060) and in men and women (8.44 vs. 11.34 μg/mL, p=0.67). ADIPOQ SNPs rs17300539 and rs266729 did not influence levels of HMW-adiponectin. Robust correlation analyses revealed a significant positive correlation between HMW-adiponectin and HDL-c (r=0.45; 95%CI: 0.27–0.59), similarly in normo- and hyperglycemic participants (p>0.99). This association was substantially attenuated in robust linear regressions adjusted for age, gender and adiposity.

Conclusions: Adiponectin levels in this population were not determined by the commonest SNPs of the adiponectin gene, were unaffected by glycemic status; but were significantly correlated with HDL-c levels. Previous studies have attributed some of the beneficial effects of adiponectin to its effect on HDL-c.

Open access