Larry's AIDS Case History

This page describes my HIV/AIDS experience in terms of
laboratory measures, therapies and HIV-associated illnesses.

I was diagnosed HIV positive in November of 1988. I started AZT therapy in July 1989. Since then, I have switched or added drugs as they became available (see Table 1). This "aggressive approach" had little effect on the declining pattern of my CD4 cell count (see Figure 1) until introduction of a protease inhibitor. To manage my HIV disease today, I'm on a twice daily combination of four antiretroviral medicines.

HIV/AIDS-associated infections

The first manifestation of my HIV infection was in the form of shingles (Herpes Zoster) in April 1990. These painful skin lesions spread following nerve pathways. Although anyone (who has had chicken pox) can get shingles, they occur more frequently in the elderly and immune-compromised. I required treatment with IV acyclovir to resolve this infection. Since then, I have had minor problems with oral candidiasis and various skin infections. The major opportunistic infections that I've had were a molluscum skin infection and AIDS-associated CMV retinitis.

Molluscum contagiosum is a viral skin infection which causes wart-like lesions. It is transmitted by direct contact, either sexual or nonsexual. The infection usually resolves itself in healthy people within 6 months to 2 years without treatment. In severely immunocompromised people the infection is often chronic, requiring treatment by freezing or surgical removal of lesions.

For me, molluscum lesions were all over my body but reached near-confluent levels on my neck and crotch. Despite aggressive (and painful) routine treatment, by January 1996, the infection could no longer be controlled.

"Showing off" my
central venous catheter along
White Rock Lake
in Dallas

CMV is a virus transmitted by bodily fluids and can be transmitted from mother to fetus. In more developed counties like the United States, around 40% of adults have been exposed to CMV, while in developing countries nearly all have. In healthy adults, primary CMV infection causes a mononucleosis like syndrome. CMV infection usually manifests in HIV patients with CD4 counts less than 50. The most common presentation of CMV in AIDS is retinitis but it can cause infections in the gastrointestinal tract, brain, and heart. In CMV retinitis, the virus destroys the retinal cells of the eye.	Anatomy of the eye
There is no cure for CMV retinitis and until recently, a CMV retinitis diagnosis meant disease treatment and management by daily infusions of antivirals for life. When the infection becomes active and vision is threatened, antivirals are often directly introduced into the vitreous humor by intravitreal injection. The IV antivirals most commonly used to treat active CMV retinitis are ganciclovir (Cytovene) and foscarnet (Foscavir). Cytovene use commonly results in severe neutropenia, requiring discontinued drug use or a costly intervention with human granulocyte colony stimulating factor (G-CSF, Neupogen). Foscarnet causes some degree of renal impairment in most patients. Alternative treatments have recently become available but all CMV therapies are very expensive and have finite efficacy in patients with very low CD4 counts. The best way to manage chonic CMV infection now is immune reconstitution via HAART .	Retina as viewed from the pupil
Normal retina	Necrosis and pigment epithelial atrophy due to advanced CMV retinitis

My CMV was diagnosed on november 1994 and has required intravitreal injections as-well-as infusions of ganciclorvir and foscarnet to slow disease progression. I received daily infusions of these toxic IV antibiotics through in-dwelling central venous catheters for nearly two years. The presence of the catheters made me more susceptible to septic infections (infections in the blood). I had three major central line infections including one that required hospitalization. My IV ganciclovir therapy caused neutropenia resulting in my routine use of Neupogen. Despite these aggressive therapies, CMV has rendered me completely and irreversibly blind in my right eye. The side effects of my CMV retinitis included a retinal detachment requiring a vitrectomy followed by a silicone oil implant. The silicone oil replacement of my vitreous humor resulted in a hypermature cataract and glaucoma. These ocular comorbidities eventually caused unmanageable eye pain and redness. In Jan 99 my right eye was removed and a few months later I was fitted with an ocular prosthesis.

Escaping HIV at Yosemite National Park!

In March 1996, the HIV protease inhibitor Norvir (ritonavir) was approved by the FDA. Upon it's availability and with a CD4 count of only six, I started taking Norvir in combination with Zerit (d4T) and Epivir (3TC). My HIV viral load became undetectable within six weeks and my CD4 count began to rise (see graph below). My CD4 count raised above 100 for the first time in over four years and my HIV viral load has remained undetectable. My molluscum went into remission and I was able to stop CMV treatments.

HAART has been a double-edged sword for me, although it has restored my immunity, it has also resulted in high levels of triglycerides in my blood and loss of subcutaneous fat from my face.

My HIV viral load remains undetectable
but my CD4 count is depressed due to cancer radiation & chemotherapy in the summer of 2007.

Our fight for effective treatments must continue
since the problems of intolerable drug side effects and antiretroviral resistance
both impose current treatment obstacles and loom in our future!

Table 1
Dates	Antiretroviral Drug	Precipitating Event
7/89-4/91	Retrovir monotherapy (zidovudine, AZT)	CD4 < 200
4/91-6/91	HIVID monotherapy (zalcitabine, ddC¹)	CD4 < 100
6/91-12/92	AZT + ddC	none
12/92-7/93	AZT + Videx (ddI, didanosine)	elevated liver enzymes or peripheral neuropathy
7/93-8/93	ddI monotherapy	low WBC
8/93-10/93	ddI + Zerit (d4T¹)	d4T availability
10/93-11/94	d4T monotherapy	elevated liver enzymes or peripheral neuropathy
11/94-3/96	d4T + Epivir (3TC¹)	3TC availability
3/96-1/01	d4T + 3TC + Norvir (ritonavir)=HAART	Norvir availability
1/01-3/06	AZT + 3TC + Kaletra
3/06-now	Reyataz/Truvada/Norvir	elevated blood lipids
¹ddC, d4T, and 3TC were started as 'open-label drugs' prior to their FDA approval (an expanded access program to accelerate availability of new drugs)

Figure 1

The following graph plots my number of CD4-positive T lymphocytes since the time I was diagnosed HIV positive. Normal CD4 numbers for healthy, immunocompetent people range from 1000 to 1500. The current CDC definition of AIDS include individuals who are HIV positive and have a CD4 count less than 200. Note that my CD4 count was 290 the first time that this test was done. This information suggests that I was exposed to HIV substantially (years) earlier than when I was diagnosed HIV positive.