For example there is documented cross protection in other viral infections: HSV-1 can interfere with the expression of Human Papillomavirus (HPV-18) genes in cells by reducing the amount of papillomaviral mRNA when they are infected concurrently with HPV and HSV?
Pre-existing HIV-specific T cells responses in unexposed individuals may slow disease progression if infection happened. However, so far there is no evidence that this would mediate complete resistance to HIV infection. Resistance is only mediated through the genetic mutation of the co-receptor of HIV (CCR5); CCR5delta32. This mutation can be found in lucky people which are less than 1% of northern europeans who are homozygous carriers and are immune to HIV infection. Here is a link for the nice story of the Berlin Patient: http://defeathiv.org/berlin/
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