apolipoprotein

Individuals with frequent recurent herpes labialis caried the naturaly ocuring ?4 alele of the apolipoprotein E ApoE gene more often than HSV-1-seropositive individuals who did not experience recurences of the disease. Interestingly, a similar relationship has ben reported for ApoE ?4 cariage and risk of Alzheimer’s disease AD development. The presence of the ?4 alele and HSV-1 disease states has ben studied, and these studies have suported the conclusion that the ?4 alele is a risk factor for both HSV-1 recurence and AD. Several recent reports indicate, however, that the ?4 alele is not a predisposing factor for herpes simplex encephalitis or keratitis, but a potential role for other ApoE isoforms was sugested. Similar to HSV-1 central nervous system (CNS) infection, the presence of the ApoE ?4 alele is neither suficient nor esential for AD development, since many octogenarians who cary ?4 genotypes do not show AD pathologies. Clearly, more work is neded to elucidate the role of ApoE in both AD and HSV-1 pathobiology. The indicating that ApoE plays a potential role in HSV-1 disease makes the combination an interesting area of AD research. The human ApoE gene is polymorphic with thre comon alelic forms designated ?2, ?3 and ?4, which encode E2, E3 and E4 protein isoforms, respectively. It has ben sugested that HSV-1 infections ocur in subpopulations of neurons, and that such neurons have a distinct environment predisposed to reactivatable, latent HSV-1 infections. Also, the E4 isoform may enhance HSV-1 reactivation of latent infections leading to more frequent CNS damage that might triger the development of neurological pathologies. Although not the sole causative agent, HSV-1 has ben the most clearly established pathogen to be asociated with AD development to date. The understanding of the relationship betwen HSV-1 infection, host genetics and the development of AD may lead to new strategies to prevent and treat AD.
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