Vitamin D inhibits HIV, mycobacteria

Vitamin D Inhibits Human Immunodeficiency Virus Type 1 and Mycobacterium tuberculosis Infection in Macrophages through the Induction of Autophagy

Grant R. Campbell1, Stephen A. Spector1,2*
1 Department of Pediatrics, Division of Infectious Diseases, University of California San Diego, La Jolla, California, United States of America, 2 Rady Children’s Hospital, San Diego, California, United States of America
Author Summary Top

Macroautophagy (autophagy – ‘self-eating’, lysosome-dependent degradation and recycling of the intracellular components in response to stress) is an important host defense mechanism against viral and mycobacterial infections. Recent studies have described that activation of autophagy in macrophages reduces the viability of Mycobacterium tuberculosis and HIV due to an intimate autophagy-phagocytosis interaction. Low serum levels of the 25-hydroxycholecalciferol form of vitamin D have been associated with an increased risk for active tuberculosis and HIV disease progression as well as M. tuberculosis susceptibility. In this study, we report that the active form of vitamin D, 1α,25-dihydroxycholecalciferol inhibits the replication of HIV and M. tuberculosis in a concentration dependent manner. Moreover, by inhibiting key stages in the autophagy pathway, we demonstrate that the inhibition of HIV and mycobacterial growth during single infection or dual infection is dependent not only upon the induction of autophagy, but also through phagosomal maturation. Furthermore, through the use of RNA interference for the human cathelicidin microbial peptide we demonstrate that cathelicidin is essential for the 1α,25-dihydroxycholecalciferol induced autophagic flux and inhibition of HIV replication and mycobacterial growth. These findings suggest that the induction of autophagy has the potential to be useful in the treatment of persons co-infected with HIV and M. tuberculosis.

In the old days, tuberculosis patients were sent to sanatoriums, typically at high altitude, for lack of any better treatment. (See Mann’s The Magic Mountain.) As far as I know, it was thought that the mountain air did them good, but it seems more likely that greater solar exposure at high altitude and subsequent vitamin D production could have been at work. I don’t know whether anyone has looked into this.


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Steve Parker, M.D. says June 14, 2012

Phoenix, Arizona, had lots of TB sanataria in times past. Elevation is only 1,100 feet above sea level but certainly lots of sunlight!

I wonder of TB victims were sent away as an infection control measure, more than anything else.


Anonymous says August 19, 2012

Interview with John Sbarbaro:
What did sans do? They took somebody with a contagious disease who could spread it to ongoing new recipients of the disease right? Infect new people and put them in a place where they couldn’t spread the disease. It did immense good to society. Now, did it do any good for the individual? You gained weight, looked healthier but you died at the same rate as if you had been in your home. But the high altitude argument is a little more interesting because what we recently found out is that absence of oxygen or in lower oxygen tension like would have occurred on the tops of some of these mountains, the macrophages in the lungs are more active and more able to control the TB bugs. Did bed rest work? Not a chance. But it gave the physician total control… the patient couldn’t get out of bed unless you said it was OK. Couldn’t make a phone call to their family unless you said it was OK. Couldn’t have a bowel movement in a bathroom unless you said it was OK and the san director surrounded by an entourage of folks would sweep
through the halls making decisions. It’s great sense of power. Patients, if you think about it, needed that feeling of awe and respect because it gave them hope.

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