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 in disease progression, particularly for those who have a high prevalence of chronic and recurrent acute infections and poor access to medical care.  Often, survival depends upon the initial AIDS-defining illness.  Co-infection with DNA viruses such as HTLV-1 , herpes simplex virus-2 , varicella zoster virus and cytomegalovirus may enhance proviral DNA transcription and thus viral load as they may encode proteins that are able to trans-activate the expression of the HIV-1 pro-viral DNA.  Frequent exposure to helminth infections, which are endemic in Africa , activates individual immune systems , thereby shifting the cytokine balance away from an initial Th1 cell response against viruses and bacteria which would occur in the uninfected person to a less protective T helper 0/2-type response.  HIV-1 also promotes a Th1 to Th0 shift and replicates preferentially in Th2 and Th0 cells.  This makes the host more susceptible to and less able to cope with infection with HIV-1, viruses and some types of bacteria. Ironically, exposure to dengue virus seems to slow HIV progression rates temporarily.
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