A note on HIV and inflammation
It is normal for the body to respond to a viral infection by triggering inflammation within the immune system. People experience the resulting inflammation as fever, chills, sore throat, swollen lymph nodes, fatigue and so on. Inside the body much is going on as the immunological equivalent of red alert begins. Cells of the immune system are mobilized, activated and sent to sites of infection. Lymph nodes swell as the invading germ is captured, analysed, and in response the immune system makes cells with different functions—some to directly attack the virus and virus-infected cells, some to help coordinate the attack, and others to try to amplify the immune response against the virus.
In the short term, these are all generally useful steps against viruses such as those that cause the common cold or flu. However, continued inflammation and activation of the immune system over the long term carries the capacity to injure key organs and systems within the body.
Among HIV-negative people, chronic inflammation has been linked to an increased risk for cardiovascular disease, type-2 diabetes, lung disease and so on. It is very likely that the chronic inflammation detected in HIV-positive people also plays a role in these other conditions or co-morbidities.
An essential part of keeping HIV-related inflammation low is to take potent combination therapy for HIV (commonly called ART or HAART). Taking ART exactly as directed should help people acquire virological control of HIV; that is, the production of new viruses should be kept as low as possible. This means that regular viral load measurements are below the threshold where they can be accurately counted; that is, less than 50, 40 or 20 copies/ml, depending on the viral load test that is available.
However, ART cannot completely eliminate HIV-related inflammation, as HIV-infected cells continue to produce small amounts of virus deep within the body: in the lymph nodes and lymphatic tissues, within the brain and possibly bone marrow, and occasionally in the genital tract.
This ongoing production of HIV, particularly within lymph nodes and tissues, likely causes low-level continuing dysfunction within the immune system, inflammation and prolonged activation of its cells. Therefore, additional measures are needed to help further suppress inflammation. These measures will of course differ from one HIV-positive person to another but generally include the following:
- quitting smoking
- treatment of co-infections such as hepatitis B and C viruses
- regular screening for sexually transmitted infections and treatment where necessary
- maintaining a healthy weight
Clinical trials to find ways of further suppressing HIV-related inflammation are being considered or are underway. In the future, TreatmentUpdate or CATIE News will bring results from these clinical trials.
—Sean R. Hosein
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- Erlandson KM, O’Riordan M, Labbato D, et al. Relationships between inflammation, immune activation and bone health among HIV-infected adults on stable antiretroviral therapy. Journal of Acquired Immune Deficiency Syndromes. 2014 Mar 1;65(3):290-8.
- Eckard AR, Jiang Y, Debanne SM, et al. Effect of 24 weeks of statin therapy on systemic and vascular inflammation in HIV-infected subjects receiving antiretroviral therapy. Journal of Infectious Diseases. 2014; in press.
- Kuri-Cervantes L, de Oca GS, Avila-Ríos S, et al. Activation of NK cells is associated with HIV-1 disease progression. Journal of Leukocyte Biology. 2014; in press.
- Dillon SM, Lee EJ, Kotter CV, et al. An altered intestinal mucosal microbiome in HIV-1 infection is associated with mucosal and systemic immune activation and endotoxemia. Mucosal Immunology. 2014; in press.
- Westhorpe CL, Maisa A, Spelman T, et al. Associations between surface markers on blood monocytes and carotid atherosclerosis in HIV-positive individuals. Immunology and Cell Biology. 2014 Feb;92(2):133-8.
- Ng B, Macpherson P, Haddad T, et al. Heart failure in HIV infection: focus on the role of atherosclerosis. Current Opinion in Cardiology. 2014 Mar;29(2):174-9.