Mother-to-Child Transmission (MTCT) of HIV and Drugs of Abuse in Post-Highly Active Antiretroviral Therapy (HAART) Era

• Published in: Journal of neuroimmune pharmacology 2010-12, Vol.5 (4), p.507-515
• Main Authors: Purohit, Vishnudutt, Rapaka, Rao S., Shurtleff, David
• Format: Article
• Language: English
• Subjects: Antiretroviral drugs; Antiretroviral Therapy, Highly Active; Biomedical and Life Sciences; Biomedicine; Cell Biology; Drug therapy; Female; HIV - drug effects; HIV Infections - drug therapy; HIV Infections - transmission; Human immunodeficiency virus; Humans; Immunology; Infectious Disease Transmission, Vertical - statistics & numerical data; Invited Review; Neurosciences; Pharmacology/Toxicology; Pregnancy; Prenatal Exposure Delayed Effects; Prevalence; Street Drugs - adverse effects; Substance-Related Disorders - complications; Substance-Related Disorders - epidemiology; Virology
• ISSN: 1557-1890; 1557-1904
• DOI: 10.1007/s11481-010-9242-7

In the pre-highly active antiretroviral therapy (HAART) era, prenatal “vertical” mother-to-child transmission (MTCT) of HIV was about 25% and exposure of pregnant mothers to drugs of abuse (illicit drugs and tobacco smoking) was a significant contributory factor of MTCT. However, with the introduction of HAART, the rate of MTCT of HIV has decreased to less that 2%. But, it is estimated that currently about 5.1% of pregnant women use illicit drugs and 16.4% smoke tobacco. The residual prevalence of MTCT is of concern and may be related to this continued prevalence of substance use among pregnant mothers. In this report, we review and present evidence that supports the hypothesis that drugs of abuse do have the potential to increase MTCT of HIV in the presence of HAART. Exposure to drugs of abuse during pregnancy may increase MTCT of HIV through a variety of mechanisms that are addressed in detail including possible damage to the placenta, induction of preterm birth, and increasing maternal plasma viral load though a variety of putative mechanisms such as: (a) promoting HIV replication in monocyte/macrophages; (b) increasing the expression of CCR5 receptors; (c) decreasing the expression of CCR5 receptor ligands; (d) increasing the expression of CXCR4 receptors; (e) increasing the expression of DC-SIGN; (f) impairing the efficacy of HAART through drug–drug interaction; and (g) promoting HIV mutation and replication through non-adherence to HAART.