Five Quarts: A Personal and Natural History of Blood (25 page)

To the other physiological extreme is erectile dysfunction, for which several well-advertised treatments are available. Drugs such as Viagra and Cialis, contrary to popular belief, neither increase libido nor trigger an immediate erection. Rather, they depend on a key ingredient not in the pills: arousal. But once that’s fired up, Viagra, for example, stimulates the release of a chemical that increases blood flow to the penis while also inhibiting an erection-wilting enzyme.

Now, returning to women: The clitoris, unlike the multipurpose penis, exists solely for pleasure. I can think of no other body part where so little blood does so much good. Engorgement exposes the clitoris, normally hidden within the vulval cleft, and amplifies the sensitivity of its eight thousand nerve fibers—twice the number found in the entire penis, in a much smaller area. Though blood is the common agent, erection and engorgement are significantly different processes, as science writer and author Natalie Angier clarifies in
Woman: An Intimate Geography
(1999). Because the clitoris does not share the penis’s distinctive outer plexus of veins, its vascularization is more diffuse. Hence, when the clitoris swells—typically to twice its size—the outflow veins are never compressed, and so “the organ does not become a rigid little pole,” as Angier cheekily points out. This free flow of blood may be what allows the clitoris to relax and distend again and again, she adds, giving rise to the multiple orgasm.

You must be
brought to
it. It must be
reached.
And in order to be fully felt and appreciated, an orgasm depends on the hot, twisting passageways of the bloodstream. In the build to climax, the hormone oxytocin is launched into the blood in a double volley from the brain and either ovaries or testes. The surge peaks at orgasm, reaching up to five times the normal concentration. By causing heart rate and blood pressure in the typical person to double, oxytocin accelerates its own speedy travels through the body. Most pleasingly, it helps trigger the pelvic shudders that women experience during orgasm and possibly the muscular contractions in men.

Love poets have long rhapsodized how souls touch during lovemaking, and oxytocin may well be the biochemical basis for this claim. The hormone, known to be vital in forging the adamantine bond between a mother and her child (and also that between father and child, probably), may perform a similar function in sexual partners, researchers believe. Oxytocin-spiked blood stirs immediate feelings of connectedness to the person with whom you are intimate, which may either lay the foundation for long-lasting ties or, if you’re already well acquainted, strengthen existing ones. In a remarkable sense, then, oxytocin is part of the blood’s formula for building familial bonds with those who aren’t blood kin.

But blood at orgasm is not just relationship-minded, so to speak. At the same time it helps curl your toes, oxytocin signals other chemicals to gush forth, such as potent opiates aimed more at dulling sensation than amping it. These are of the same family as the endorphins released during exercise and have, for example, the effect of temporarily numbing raw nerve endings in people with migraine, arthritis, or peripheral neuropathy. Furthermore, oxytocin activates mechanisms that help heal wounds and raises blood levels of immunoglobulin, a microbe-fighting antibody. So significant are these and other benefits that, experts agree, not only is sex good for you, but it may also lead to your living longer.

Of course, those same experts are not saying, when you’re sick, have lots of sex. The heat of passion and the heat of illness do not usually overlap. And for good reason. When you’re sick, the blood is rigged to make you drowsy. Hypnos, the god of sleep, almost always thwarts Eros. You need only have a cold to appreciate this. Or, for the sake of illustration, say you’ve got a flu bug—nothing too serious, but enough to confine you to bed. While you rest, white blood cells directly attack the infection and, launching a broader assault, the body changes its internal environment to make itself less accommodating to invaders. Cellular messengers called pyrogens—“fire starters,” roughly translated—are sent through the blood to the body’s thermostat, the anterior hypothalamus in the brain, which turns up the heat. At the same time, blood vessels in the skin narrow, reducing sweating, which is a major way body heat escapes. Now producing more heat than it can lose, the body runs a fever. (By the way, for most people, what’s widely considered the normal body temperature, 98.6 degrees Fahrenheit, actually isn’t. An enduring math error from the 1800s is the cause of this misconception. The true average is 98.2.) Fever, which helps kill whatever virus or bacterium swims within, may be “a lovely way to burn,” as Peggy Lee crooned, but, truth be told, it’s lousy for lovemaking.

Even if there weren’t such sound immunological explanations for the lost carnal itch, common sense should tell you plenty: You could be contagious. You shouldn’t overexert yourself. You look like the unfed undead. And naturally, your sex appeal suffers, too. But once you or your bedmate have bounced back to health, desire follows. I’m sure almost anyone can appreciate sex after illness—the first romp, say, after your once-yearly flu—but I believe you have to have known serious illness or injury to truly savor it. As a broken bone is said to be stronger once mended, so, too, is lust restored.

Many times in Steve’s and my relationship, our sex life has had to be packed away. His meds have often been to blame. One drug dried his skin so terribly that his lips bled, making kissing out of the question, and others, designed to free him from physical pain, distanced him from good sensations. Over the years many of his prescriptions have come with the warning label
THIS DRUG MAY IMPAIR YOUR ABILITY TO OPERATE MACHINERY,
without ever noting that the machinery included his own.

But the body usually gets used to drug side effects over time—if there’s time. The most difficult period for Steve came during our third and fourth years together. During a long bout of wasting syndrome, he’d steadily lost a frightening amount of weight and, as he now reflects good-naturedly, his libido went down the toilet, too. On his doctor’s orders, I began giving him regular injections of testosterone enanthate, not to help him reclaim virility but just so he could hold on to some of his mass. Still, he got so thin that he could no longer wear the ring I’d given him on our first anniversary. Everything began to change for the better, finally, thanks to new medications. Steve’s T cells rose, he gained weight, the color came back to his face, his appetites returned. We had no idea how long he’d remain stable, which, as I see now, gave sex an intensity that was bittersweet.
This might just be a reprieve,
I thought, just a short break of sun. To this day I’ve never been able to shake that feeling.

The first time back out can be a little awkward at first. Naked, you feel unusually exposed. Skin is the body’s largest organ, a marvelous complex of nerve endings, sweat glands, and the tiniest of blood vessels, the capillaries. At any given time, about one-quarter of the body’s blood flows through the skin. Even so, it may take a moment to warm up, to get the blood moving. My partner and I remove our clothes and reach for each other as if underwater, two bodies meeting at the bottom of a pool. Pushing against resistance, we kick our legs to stay in place, hold our breath, close our eyes. Just as we make contact, we surface, mouth to mouth among the waves.

T
HIRTEEN

Memory Cells

SHORTLY AFTER STEVE AND I BEGAN LIVING TOGETHER IN early 1990, we cemented our coupledom by making deposits into a joint savings account. The money wasn’t earmarked for a future vacation or a down payment on a home. This was our cure fund, a stash of cash set aside for the day the magic bullet would be discovered. We knew Steve’s health insurance wouldn’t immediately cover a brand-new treatment, no matter how miraculous. And for some strange reason, we both felt sure the cure would be found overseas. On a moment’s notice, we’d have to board a plane to who knows where. Steve thought it might be Japan. I thought France. Hungry for news, we attended the monthly Project Inform updates held in a church in the Castro. As in an old-fashioned town-hall meeting, anyone could stand up and speak, share treatment success or horror stories, or ask questions of the evening’s guest—a visiting doctor, usually. Oftentimes, though, lively debate devolved into medico-babble few of us in the creaking pews could follow.

I remember how, in June of that year, everyone was talking about an “amazing” and “promising” experimental therapy called hyperthermia, or blood boiling. Sure, it had only been tried on two people, but the basic science behind it sounded pretty solid. The opposite of hyp
o
thermia—the condition suffered by people who plunge through thin ice—hyp
er
thermia mimicked a high fever, the body’s infection-fighting mechanism. The procedure involved withdrawing the blood from an AIDS patient’s body, pint by pint, using an apparatus that was a crude forerunner of today’s blood bank e-chair. The blood was heated to up to 115 degrees Fahrenheit, thus killing the virus, then cooled and returned to circulation. The procedure, performed by an Atlanta doctor, took a mere two hours. One of his two treated patients went on national TV and declared himself cured of AIDS—an overstatement, yes, but his viral activity had in fact dropped significantly and his T cells had shot up. Soon thereafter, though, the blood boiling fever broke. A third patient died from the procedure, and government investigators promptly deemed hyperthermia dangerous, worthless, and done with. As it turned out, what we’d all conveniently forgotten in the excitement was that HIV takes up residence not just in the bloodstream but in organs and the glands of the lymph system. So the blood would inevitably be flooded with new virus; it was just a matter of time.

In the spring Steve had started taking AZT, the sole FDA-approved drug at the time, and he’d begun seeing a new physician, a Spanish-born woman recommended by a friend at Project Inform. Our first impression of Dr. Inmaculada Marti was that she had turned what would’ve been just another drab office in the Davies Medical Center into a glistening cavern. The space was a geode—the shelves, windowsill, and her whole desk covered with crystals, save for a tiny spot reserved for her prescription pad. Steve stuck with her for about nine months. She recommended acupuncture, which he tried, and at every office visit, while I watched from the rose quartz section, she would spend a lot of time examining his tongue. As his immune system staggered, Dr. Marti seemed to get angry first at the lab results, then at Steve, as if he were an uncooperative patient. “You’re taking an antiviral,” she bristled during one appointment, “so why do you have virus?” She started him on an alternative therapy, Iscador, an extract of mistletoe, which she ordered from Switzerland. In the end, however, we knew she’d run out of tricks when she proposed sending a sample of Steve’s blood to New Mexico, where, for four hundred dollars in cash only, a colleague would perform a “visual study” of his virus and cells. How would the equivalent of a tarot card reading of Steve’s T cells help steer his treatment? Dr. Marti admitted she couldn’t say.

After switching to a new doctor, a wonderful woman firmly grounded in Western medicine, Steve, over months, then years, worked his way through the latest antivirals—ddC, ddI, d4T, 3TC—all bleached-white tablets, like generic aspirin. By contrast, I remember how very different Steve’s first protease inhibitor looked. Saquinavir came wrapped in bright gold-and-green capsules, plump and shiny like movie candy.

I once read an article on how pharmaceutical companies create the names for their forthcoming products, a skill requiring sales savvy and a gift for poetry. Experts invent words aimed to evoke just the right feeling, mood, quality, or image. The best-named drugs seem to start working just by saying their names. Say it slowly again and again and the sleep aid Ambien becomes a lulling chant. And it’s no coincidence, I’d wager, that Viagra is so close to Niagara, that mighty flow of fluid. To me, the names given to the protease inhibitors seemed intended to call to mind fabled heroes of an earlier time. One after the other they arrived, modern-day Knights of the Round Table: Saquinavir, Ritonavir, Nelfinavir, Crixivan.

In the Arthurian legend, as Steve recently pointed out to me, more than a hundred knights earned a place at the Round Table, but a single seat, or “siege,” remained empty: the Siege Perilous. It could be filled only by the true finder of the Holy Grail and would bring death to any pretender. Though the notion of killer furniture seems silly to me, I do love the element of the waiting chair. This says so simply that the right person just hasn’t arrived yet. One day, the Siege Perilous will be occupied.

I SPOKE WITH DR. JAY LEVY ALMOST TWENTY YEARS TO THE DAY after he had co-discovered the virus that causes AIDS. When I first mentioned the milestone, though, he seemed a little surprised at the math. “Oh, that’s right,” he said, brightening, doing his own mental tally. “That’s right, twenty years.” Levy, who heads the Laboratory of Tumor and AIDS Virus Research at the University of California, San Francisco, added that he’d actually made the September 1983 discovery in a lab right across the hall from the small office where we were seated. But, he noted, it’s now gone.

I leaned back in my chair and glanced across the hallway, compelled by that queer human reflex to look for something we’re told is not there.
What is it that we think we’ll see?

“They took the room,” Levy added.

“Someone ‘took’ the room?”

“The Smithsonian, yeah.” A bemused twinkle lit his gray-green eyes. “They came in and just took the whole thing, where we’d isolated the virus. The lab hood, my lab jacket, my notebooks, everything. The sign on the door. One day it’s going to be in the Smithsonian.”

As he continued the tale, I realized that, to him, the furniture and equipment hadn’t been so much historical as old and in the way. What seemed to truly please the sixty-four-year-old scientist was that the university renovated the lab, providing him a tidy new space for his ongoing research.

Finding HIV was one thing. “Conquering this virus,” as he put it, has occupied him since. In the mid-1980s, for example, Levy developed a technique for inactivating HIV in the clotting factor preparations used by hemophiliacs. “Then I became sort of an expert with blood products—
How do you get rid of HIV without destroying the proteins you’re dealing with?
” It’s a good indication of the man that he modestly describes this work as “helping out.” Levy’s pioneering heat treatment method, adopted by the blood products industry, has saved many lives.

Levy, author of the seminal text
HIV and the Pathogenesis of AIDS
(1994), among other books, was also the first scientist to report that HIV could cross the blood-brain barrier, the filtration system that normally protects the brain from harmful substances carried in the bloodstream. To me, the term
blood-brain barrier
had always given the impression of a single dam-like structure at the base of the skull, where I’d imagined it was located, but the barrier is actually the layer of tightly packed cells that make up the walls of all brain capillaries. Levy correctly concluded that HIV’s ability to pass through this barrier led to neurological diseases such as AIDS-related dementia. Since some of the earliest available anti-HIV drugs did not cross the blood-brain barrier, his findings underscored the necessity of developing drugs that could.

I had met Dr. Levy in person once before today. In this same building, eleven years earlier and twelve floors below, standing before six hundred people in a five-hundred-seat lecture hall, he and two other prominent researchers had spoken at a public forum I’d organized as a staff member of the San Francisco AIDS Foundation. The free event was the kick-off for my 1992 “Be Here for the Cure” media campaign. Like the campaign, the forum was a look forward. The topic: prospects for a cure. As the event was about to get under way, I adjusted the lectern microphone and scanned the packed auditorium, a great throng of gay men, mostly. People stood in the back, jammed the aisles, and sat on the floor before the stage where Marcus Conant, the pioneering AIDS physician; Mathilde Krim, cofounder of amfAR; and Levy were seated. I spotted Steve, who was saving a place for me on the stairway, and went to join him.

Both the setting and the stature of the speakers gave this gathering a different feel from the frantic town-hall meetings of two years earlier. The mood had changed, too. It was as if, finally, science had given hope a scaffolding to build on. Dr. Conant spoke about a new treatment strategy, “combination therapy,” now standard protocol, and reported how taking prophylaxis against Pneumocystis pneumonia increased life expectancy. Dr. Krim talked about promising vaccines under development. But the night’s big bombshell came from Dr. Levy. “I do not believe that everyone infected with HIV will come down with symptoms,” he told the crowd. He then described a “blood factor” he was investigating and predicted the day when a devastated immune system could be restored to full fighting strength.

Dr. Levy remembers that evening well, though, as he admitted to me in his office, he has never really liked the word
cure.
“
Cure
is not the word.
Control
is the word,” he stressed. Though significantly grayer than when I’d last seen him, Levy spoke with the same certainty. “You aren’t gonna kill every damn cell affected in the body. HIV is a virus like herpes that you have forever. But we
will
regain control of it.”

To reach this end, Dr. Levy has spent the bulk of his energy over the past seventeen years studying a small pool of research subjects: those rare individuals with HIV known technically as long-term nonprogressors or, more commonly, long-term survivors. Statistics indicate that only about 1 percent of the infected fall into this category.

“We first started to look at these people back in 1986 and found that the virus in them couldn’t replicate,” he recalled. The subjects also had relatively normal white blood cell counts. In those early days, without drug therapy, most people diagnosed with AIDS declined rapidly. “But these were healthy people who showed no signs of infection. And we asked,
What’s the secret?
”

For answers, Levy, a trained virologist, crossed over to a new turf, immunology. “One of the things with viruses,” he explained, “is that, to survive, they have to exist within a hostile environment.” The brunt of this hostility comes from the body’s natural antiviral response. After HIV invades, antibodies produced by B cells, the fleet of T cells, and other weapons of immunity flood the bloodstream, mounting a formidable defense. But inevitably, in nearly every case, the immune system is soon turned against itself as viral RNA commandeers helper T cell DNA, or, simply put, the helper cells become factories, churning out more copies of HIV.

Not, however, in the bodies of nonprogressors.

In these lucky individuals, Levy found, the internal environment remains antagonistic to HIV, not simply for weeks or years but, in some, for decades. On this topic, I realized I had been operating under a misconception. By virtue of these survivors staying symptom-free, I’d assumed that, within them, all was weirdly peaceful—a milieu wherein HIV and white blood cells quietly coexisted.
Don’t bother me, I won’t bother you.
Not true. Nonprogressors’ immune systems actually contain supersoldiers whose secret weapon, Levy discovered, is a chemical substance he named CD8 Antiviral Factor, or CAF.

CAF is a protein produced by a type of T cell called the CD8 lymphocyte, or suppressor cell. (These white blood cells don’t “suppress” invading organisms but, rather, inhibit the activity of fellow cells within the immune system.) As Dr. Levy explained, while CAF does not stop HIV from infecting helper T cells, “It blocks the virus so it can’t make its RNA. HIV is shut off by this factor.”

Everyone has CAF, I was glad to hear him say; however, he believes that “only long-term survivors have a capability of maintaining it.” The hope for HIV progressors—my term—is learning how to provoke or rekindle CAF production and maintain it over time.

But first, Jay Levy must actually find this elusive protein. While prominent AIDS researchers agree with him that an antiviral factor is produced by CD8 cells, Levy has yet to isolate it. On the one hand, he and his team can extract a sample of blood from a nonprogressor that contains this factor and can demonstrate in the lab that it does in fact suppress the virus. But where exactly is it? “I can’t yet give you the molecular structure of CAF,” Levy said evenly, the very picture of unruffledness. It is this quality, I realized at that precise moment, that separates the true scientists from the test-tube throwers. Since 1989 the Levy team has been on a molecular scavenger hunt, winnowing the possible proteins from a group of two thousand candidates down to two hundred and now down to fourteen. “These are fourteen of our best. Which, potentially, could be CAF. I don’t know. But when we find it, it’s going to be such a powerful antiviral drug and such an unusual and universal means of bringing back control to the infected person.”

I gave him a look that asked,
Should we be holding our breath?
His reply was at once apologetic and resigned: “The fact is, if we were a [biotechnology] company, we’d have the research all done by now.”

At this point in our conversation, we left his office and stepped into the adjacent lab, a functional space, but, as he accurately described it, “far from plush.” He noted that, though he’d prefer to spend all his time in here working on research, every year the struggle to obtain government and foundation grants gets tougher. “I spent 50 percent of my time last year traveling around trying to get the funds.” He sighed his frustration. “It’s not right.”