From: Billi Goldberg <bigoldberg@igc.apc.org>
Subject: Point and Counterpoint on UVR
Note: Copyright 1992, Dan R. Greening. Non-commercial reproduction allowed.
Archive-Number: 6472
Organization: unspecified
Date: Thu, 19 Nov 92 12:59:27 PST

The following letter was printed in the San Francisco Sentinel on 
Thursday, November 19, 1992. Dr. Waites writes for the Advocate, is 
involved in the Compound Q trials, and has a large AIDS practice in San
Francisco.
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            POINT: ULTRAVIOLET RAYS IN MODERATION OKAY
                          by Larry Waites

   I am writing to correct errors in your article of 12 November and 
educate you and your readers about what is known about the activation of 
the HIV virus by UV irradiation.

   First, a criticism of Dr. Conant. Both the Keith-Beer and Pacific 
Oaks Medical Groups in Los Angeles have twice as many HIV+ patients as 
does Dr. Conant's practice. He, therefore, does not have the largest 
private HIV+ practice in the world. My group, the 450 Sutter Medical 
Group, purposefully limits our practice size because we prefer to spend 
more time with our patients and not run a factors.

   Now for arguments supporting Dr. Conant. The following is an update 
recap of a discussion I present in my monthly Advocate column, 
"AIDSLINE" in July 1991.

   Most physicians remember the first reports that ultraviolet 
irradiations (non-visible rays of light) activated the HIV virus in 
vitro (S. Rasheed, M.D., Virology, 154(2), 1986, p.395). Only recently 
studies have been done in vivo using mice, showing the same results 
(Vogel, J. Journal of Virology, 1992, 66/1,(1-5).

   It has been reported the UV irradiation, but not visible sunlight, 
induced the transcription of the HIV virus--activated the virus. (B. 
Stein, M.D., Journal of Virology, 63(11), 1989, p. 4540). Dr. Stein's 
research found that the UV response of the outer layers of skin was 
magnified and spread to the deeper layers that are usually more 
shielded, including the Langerhans cells, which are known to be infected 
by the HIV virus. The most potent activation of the HIV virus occurs 
with UV-C irradiation, less so with UV-B and only slightly with UV-A. 
UV-C and UV-B are the burning rays of the sun which are most prominent 
during midday (S>K> Stanley, M.D., AIDS Research in Human Retroviruses, 
5(4), 1989, p.375). It is my impression that virtually all tanning beds 
in current use are claimed to emit pure UV-A irradiation.

   Viral activation by UV irradiation has been associated with a drop in 
viability of HIV virus infected cells, suggesting that a certain level 
of cellular stress was most likely necessary to initiate virus 
expression (S.K. Stanley, M.D.) In other words, it seems that it is 
sunburning that activates the virus.

   At our office, eosinophilic folliculitis is easily controlled by 
having the patient take Seldane 50 mg by mouth twice daily. I see no 
need for tanning therapy. Unfortunately, psoriasis, that all too common, 
horribly disfiguring skin disease which afflicts many HIV patients, is 
only controllable with the use os psoralen UV-A therapy. Also, 
unfortunately, psoralens increase the sensitivity of the HIV virus to 
activation by UV-A irradiation three-fold (Morrey, J.D., Journal of 
Virology, 1991, 65/9, p. 5045). The patient and his physician must 
weight the risks and benefits of therapy and reach a decision together 
on how to proceed.

   The bottom line is that suntanning beds should by used by HIV+ 
patients for medical therapy only. I recommend that being outside is all 
right; but a good number 8 sunblock is necessary--and absolutely no 
sunburns! It is important to remember that many of the drugs used to 
treat HIV disease make HIV+ patients more susceptible to sunburns (for 
example: Dapsone, Bactrim/Septra (trimethoprim-sulfamethoxazole), and 
possible Retrovir (AZT). Certainly most patients' eyes are more 
sensitive while take AZT>

   I hope this discussion has enlightened you and your readers and 
suggest that Mr. Goldberg's complaint is unnecessary, uninformed, and a 
useless waste of important people's time.

Larry A. Waites, M.D., M.P.H.
Research Director
450 Sutter Medical Group
San Francisco, CA
***********************************************************************
The following article was printed in the San Francisco Sentinel on 
Thursday, November 19, 1992. It is being posted with the permission of 
the author, Charles R. Caulfield.
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              COUNTERPOINT: ULTRAVIOLET RAYS ARE DANGEROUS
                      by Charles R. Caulfield

   The recent Sentinel HIV News article, "New Controversy Over HIV and 
Suntanning" drew a significant number of responses from our readers.  
Most notable among these was the response of Dr. Larry Waites, a 
physician in practice with the 450 Sutter Medical Group in San 
Francisco. His response to the article in question underplayed the 
significance of the risk of HIV viral activation by moderate exposure to 
UV radiation by use of tanning beds and exposure to sunlight. 

   Contrary to Dr, Waites statement that "virtually all tanning beds in 
current use are claimed to emit pure UVA radiation," our research, which 
included an interview with an electronics specialist affiliated with 
Sun-Days Tanning Centers, has led us to the discovery that, on the 
contrary, both UVA and UVB radiation are commonly used in the tanning 
beds which are a mainstay of the industry. It should also be noted that 
use of specialized tanning beds which emit only type A radiation, where 
they are available, cost the consumer four times the amount of the use 
of beds which utilize both UVA and UVB together. 

   In all fairness to the distinguished physician's rebuttal, a thorough 
review of the medical literature pertaining to the effect of ultraviolet 
radiation on the immune response was undertaken by this reporter.

   Principal among the Dr. Waites' erroneous allegations is the 
suggestion that UV-A radiation "only slightly" acts in a manner which 
could activate HIV expression. This is in stark contrast to an August, 
1992, article in the International Journal of Dermatology, vol.31. no. 
8, by Dobak and Liu, two Dermatologists from U.C. San Diego School of 
Medicine, in which it is stated that "Ultraviolet A is capable of 
causing various types of structural damage to DNA. It is conceivable 
that reduction of Langhans cells by UVA radiation results in inefficient 
immunodestruction of early neoplastic cells...allowing the exposure to 
be expressed in the form of tumors." pp. 544-45. . DNA damage caused by 
UVA radiation was stated August 28, 1992, article in the 
journal,Science, entitled "Awakenings...UV light and HIV gene 
activation" to be a necessary perquisite for the awakening of HIV from 
its quiescent, or dormant state.

   Issue must also be taken with Dr. Waites allegation that UV type C 
radiation is the most dangerous constituent of sunlight toward the 
immune system. This is clearly contradicted by Roberts, et al in 
"Ultraviolet radiation and modulation of the immune response" which 
appears in the text Immune Mechanisms in Cutaneous Disease,, Marcel 
Dekker, NY, 1989, in which it states "UVC is potentially the most 
harmful of the ultraviolet radiations. Fortunately, UVC does not reach 
the earths surface because it is effectively absorbed by the ozone in 
the upper atmosphere." p.170.

   Dr. Waites admittedly advises his patients that nonburning exposure 
to sunlight is "all right, but a good number 8 sunscreen is necessary." 
According to Liu and Dobak, in the aforementioned reference from the 
International Journal of Dermatology, "In the United States, many 
sunscreen formulations claim UVA protection, but in fact none of them 
block all UVA rays." p.544.

   Dr. Waites, who now practices Internal Medicine, had his training and 
early clinical practice in the field of pediatrics. It is likely that he 
does not have either the time or inclination to familiarize himself with 
the basic science associated with the most recent developments in 
immunology and dermatology. It must be reiterated once again that a 
clear link appears to exist between exposure to UVA and UVB radiation 
and immunosuppressive effects on subcutaneous Langhans cells. This 
causes an impairment  of their ability to signal the proliferation of 
CD4 cells, as well as  cellular DNA damage  resulting in acceleration of 
viral expression. This is clearly stated in the most current medical 
peer review journals, particularly "Ultraviolet B-Irradiated Antigen-
Presenting Cells Display Altered Accessory Signaling for T-Cell 
Activation", by Simon, et al in The Journal of Investigative 
Dermatology, vol. 98, no. 6, June 1992.

   In keeping with the warning issued in the October issue of AIDS 
Treatment News, and other medical journals, the community must be warned 
of the potential danger of exposure to sunlight and tanning beds, due to 
the potential for immune suppression and viral activation, which may 
play a key role in accelerating the decline and death of people living 
with HIV.

   The Dr.'s terse response to the recent Sentinel article can only be 
viewed as a justification of his own unfamiliarity with current research 
on the topic. It does seem rather odd, also, that Dr, Waites begins his 
diatribe with a cynical, if not catty reference to the clinical practice 
of an esteemed colleague, Dr. Marcus Conant, as a "factory". Perhaps, 
Dr. Waites is unaware of the fact that most of the references cited in 
this and the previous Sentinel article reached publication after the 
article he penned for the Advocate  in July 1991, the content of which 
his letter provides an "updated recap." Regardless, it is our earnest 
hope that in light of the overwhelming medical consensus as evidenced in 
peer review journals, rather than in the popular press, people living 
with HIV will avoid all immunosuppressive factors which could have 
deleterious effects on their health and chances for survival. It should 
be noted that due to the controversy surrounding use of exposure to UV 
radiation as a treatment for dermatological manifestations of HIV, 
guidelines for its use are to be drawn up by physician peer consensus at 
the December Conference of the American Dermatological Association,  to 
be held in San Francisco. The Sentinel will cover these proceedings for 
its readers.
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