Can tobacco smoke enhance HIV infectivity?

Contributed by Guest Blogger: C. Matsuoka ’14

The relationship between tobacco smoking and HIV/AIDS progression still remains controversial. HIV is a retrovirus that causes the immune system to begin to fail, leading to life-threatening opportunistic infections. Infection with HIV-1 leads to a progressive decrease of CD4+ T cell count and an increase in viral load.
Although there is no concrete evidence that tobacco smoking has a major effect on the progression of HIV-1 of AIDS, there is strong evidence that it increases the risk of becoming infected with HIV. An aqueous tobacco smoke extract (TSE) was used to study the direct effect of smoking on HIV infection and its effects on gene expression in human T cells. Data demonstrates that TSE can enhance HIV infectivity and has antioxidant potential capable of protecting cells and virions from oxidative damage. To prepare the aqueous TSE, 5 cigarettes were puffed through 40 mLs of sterile saline (PBS). Researchers plated TZM-bl cells, which express CD4 and are useful for assessments of viral infectivity, and incubated them with serial doses of TSE. The cells were then infected with HIV-1. Assessed by the MTT cell viability test, cells with low amounts of TSE showed a mild proliferative effect, whereas larger amounts showed increasing toxicity to cells. The effect of TSE on HIV production/infectivity was also tested in human Jurkat T cells (immortalized line of T lymphocyte cells). The Jurkat cells were infected with HIV-1 and then treated with either PBS or TSE. When Jurkat T cells were infected with HIV, HIV production increased over 50% following TSE stimulation, comparable to the direct HIV-simulating effect of TSE in TZM-bl cells alone. To test the ability of TSE to protect HIV virions from oxidative damage by t-BOOH, HIV-1 viral stalks were added to media containing t-BOOH, t-BOOH/TSE, and PBS control. Researchers found that TSE has antioxidant (a molecule capable of inhibiting the oxidation of other molecules) activity, protecting cells against oxidant damage. Only when TSE is present can HIV virions, exposed to t-BOOH, retain its ability to replicate at the same level as the control untreated virus. In conclusion, researchers revealed a novel aspect of the interaction between tobacco smoking and HIV infectivity. Studying the effects of smoking on HIV infectivity has the potential to reveal a novel viral activation mechanism for which inhibitors could be discovered.
Since Marlboro Lights were used to make the TSE, would there be a different effect if a different brand of cigarettes were used? Are there real life human examples of this study that would back up the data? Does tobacco smoke have this effect on other viruses as well?
 

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