role of genes in encoding chemokine receptors (CCR5 and CCR2) and chemokines (SDF-1). While CCR5 has multiple variants in its coding region, the deletion of a 32-bp segment results in a nonfunctional receptor, thus preventing HIV entry; two copies of this gene provide strong protection against HIV infection, although the protection is not absolute. This allele is found in around 10% of Europeans but is rare in Africans and Asians. Multiple studies of HIV-infected persons have shown that presence of one copy of this mutation, named CCR5-Δ32 (CCR5 delta 32) delays progression to the condition of AIDS by about 2 years. The National Institute of Health (NIH) has funded research studies to learn more about this genetic mutation. In such research, NIH has found that there exist genetic tests that can determine if a person has this mutation. Implications of a genetic test may in the future allow clinicians to change treatment for the HIV infection according to the genetic makeup of an individual, Currently there exist several at-home tests for the CCR5 mutation in individuals; however, they are not diagnostic tests. A relatively new class of drugs for HIV treatment relies on the genetic makeup of the individual. Entry inhibitors bind to the CCR5 protein to block HIV from binding to the CD4 cell. The effect of co-infections on progression rates Coinfections or immunizations may enhance viral replication by inducing a response and activation of the immune system. This activation facilitates the three key stages of the viral life cycle: entry to the cell; reverse transcription and proviral transcription. Chemokine receptors are vital for the entry of HIV into cells. The expression of these receptors is inducible by immune activation caused through infection or immunization, thus augmenting the number of cells that are able to be infected by HIV-1. Both reverse transcription of the HIV-1 genome and the rate of transcription of proviral DNA rely upon the activation state of the cell and are less likely to be successful in quiescent cells. In activated cells there is an increase in the cytoplasmic concentrations of mediators required for reverse transcription of the HIV genome. Activated cells also release IFN-alpha which acts on an autocrine and paracrine loop that up-regulates the levels of physiologically active NF-kappa B which activates host cell genes as well as the HIV-1 LTR. The impact of co-infections by micro-organisms such as Mycobacterium tuberculosis can be important