Virus can simultaneously assemble and hide in intracellular compartments, largely free from immune attack. Interestingly, the
mononuclear phagocytes are not destroyed by virus and throughout infection they still contribute to host immunity while at the same time perpetuating
lentiviral dissemination. Infected mononuclear phagocytes are readily observed in lymph nodes and organs such as the lung and brain, where they produce cytotoxic mediators that contribute to the development of disease.
For human immunodeficiency virus (HIV) infection functional impairment of infected mononuclear phagocytes likely accelerates immune deficiency. Thus, the questions most asked are how can a cell that possesses so many intrinsic defense mechanisms harbor such viral pathogens for prolonged time periods? How can mononuclear phagocytes serve both as sentries and vehicles for disseminating infection and inducing disease? Indeed, in regards to biology, both for ontogeny and phylogeny, mononuclear phagocytes are the most primitive sensors of tissue injury and as such serve to clear debris and simultaneously protect the host's homeostatic environment.
Their roles serve the host in non-specific defense (innate immunity) and in initiating cell-specific protection (adaptive immunity). A consistent evolutionary role resides in the ability of mononuclear phagocytes to engulf, digest and destroy cell and tissue debris through phagolysosomal fusion. Interestingly, mononuclear phagocytes can affect neighboring lymphocytes and other immunocytes to perform similar functions, albeit by divergent mechanisms. Control of viral growth occurs together with the MP's notable possession of a vast repertoire of immune secretory factors that include pro-inflammatory cytokines, chemokines, arachidonic acid and its metabolites, platelet activating factor, nitric oxide, quinolinic acid, amongst others. These serve to regulate immune defense, cell mobility, antigen presentation, immune activation, and cell differentiation. During disease such secretions are induced by infection and affect inflammatory processes that speed cell and tissue injury leading to clinical symptoms and morbidities. This, in the case of common lentiviral tissue injuries, leads to substantive lung, brain, blood, and joint diseases.
from Lentiviruses and Macrophages: Molecular and Cellular InteractionsFurther reading: