Received 8/5/97 Accepted 8/12/97

There is much work left to do to completely understand how M. avium contributes to the general outcome of the host response to HIV infections. However, M. avium clearly has the ability to affect various phases of host responsiveness. This is particularly important in advanced stages of the infection when mycobacterial loads are elevated and host lymphocyte populations have lost the appropriate ratios necessary to equilibrate effective cell mediated immune responses. Although there are probably other mycobacterial components associated with the growth of M. avium, it is logical to assume that lipids would be the most likely element to affect host responsiveness over a long period. This would primarily be due to the lipophilic nature and low-level of biodegradability generally associated with the complex lipids produced by mycobacteria. Because of their innate properties, certain M. avium lipids can interact with host membranes and generally disrupt overall function and stability of the cell associated with that membrane system. Disruptions like this would include not only the initially infected macrophage, but would also eventually include surrounding bystander cells such as T and B lymphocytes.

In addition, the ability to induce various cytokines and eicosanoid components allows M. avium lipids to affect the general homeostasis of the complex cytokine network necessary to program effective host responses to intracellular pathogens such as mycobacteria. Although the emphasis of this review has been the GPL components of M. avium, it is important to realize that other M. avium components may also prove to be important in the long-term effect on HIV-infected individuals. Further studies are necessary to complete the total picture and to define more fully M. avium's contribution to pathogenesis in AIDS.