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Seated in the lower right rib cage, it is the second-largest human organ (the first being the skin), and in healthy people is the size of a small football. And it favors the sucker punch. You don't know you're in trouble until it's too late.
The trouble can start when the hep B virus wends its way into the bloodstream and, to a lesser extent, semen and other secretions. Gaining entry isn't difficult. During sex, for example, the virus in ejaculate travels to a new host through anal or vaginal microabrasions, tiny ruptures that are far from rare. Once in the bloodstream, the virus hunts for home like a salmon looking to spawn. It heads for the liver, the place where it can multiply.
In science-speak, hepatitis B is a hepadnavirus, comprised of DNA, a protein core, and a lipid, or fat, envelope that surrounds it. Microscopic spikes, or "surface antigen," protrude from the envelope -- like a burr, the virus uses the spikes to attach to a liver cell.
"Most viruses are tissue-specific -- that's why you get a cold in your sinuses and not in your kidneys," says Woodruff. And the most efficient viruses, like hep B -- and unlike Ebola, for example -- have learned over a long evolution to kill their hosts slowly, thereby giving themselves a longer life.
Once the virus has attached to the liver cell, it pulls a biochemical coup: It moves into the nucleus and uses the liver cell's own replication mechanisms to create a new "progeny virus," which escapes and starts the cycle again.
In the majority of cases, the body's immune response cuts this process short, and lifelong immunity kicks in. But in the 5 to 10 percent of people who become carriers, replication never stops. And because the virus is efficient, and people get infected with more than one at a time (a contaminated needle might hold millions), the levels of virus in the bloodstream can soar to the billions per milliliter of blood.
Some experts believe that liver damage, meanwhile, is due not to the virus itself but to the inflammation that occurs when the body's immune system rushes in to defend the organ. Whatever the precise cause, the diseased liver in a "chronic active" carrier -- someone who's suffering symptoms -- grows ever smaller and more scarred, making it increasingly difficult for critical blood flow to reach the organ. In addition, a scarred liver can't properly break down and remove harmful substances, wreaking havoc in the brain, and sometimes -- as in Marx's case -- causing a coma.
The drug interferon in some cases helps reverse the disease; several other experimental drugs show promise, and two are being used in trials at San Francisco's Veterans Administration Hospital. But to date, there's no sure-fire treatment.
And the cost is enormous. According to the American Liver Foundation, the hospital tab for liver disease in 1993 reached $7.8 billion. The 3,000-plus liver transplants performed each year cost as much as $300,000 apiece.
"But many people still don't know about the disease unless someone they know has been affected," says Norma Martinez, coordinator of demonstration projects in San Francisco aimed at immunizing all newborns and a number of seventh-graders as well.
"It doesn't help that the population growing up now has never seen polio," adds the Health Department's Taylor.
When polio in the 1950s left thousands of people paralyzed, crippled, and dead, many of them children, the virus inspired hysteria. The disease wasn't sexually transmitted. No relief could be found in moralizing; no refuge could be taken in homophobic scapegoating. Mothers refused to take their children to the zoo -- polio, it was feared, was everywhere. When the Salk vaccine arrived and polio was declared eradicable, bells chimed nationwide and children lined up eagerly in school gymnasiums for their injections.
But when the latest hepatitis B vaccine was approved by the Food and Drug Administration in 1986 -- thanks to the discoveries of a UCSF biochemistry professor and the chairman of Chiron Corp., an Emeryville biotechnology firm -- barely a huzzah was heard.
Quiet, like the virus, is the progress that's been made.
"The incidence has decreased, which is wonderful," says Miriam Alter, chief of the epidemiology section of the CDC hepatitis branch. Since 1985, Alter says, the incidence of hepatitis B infection has declined, from more than 300,000 a year in 1985 to less than 200,000 a year in 1994.
"Most of the decline occurred among homosexual men as a result of safe-sex precautions," Alter says. It is a macabre irony: Pre-AIDS, hepatitis B was becoming one of the most common and deadly diseases among gay men. The early understanding of the HIV profile was helped along by researchers' experience with hepatitis B. And now because of the deadlier disease, the less potent but more ubiquitous one is dwindling. "We're riding on AIDS's coattails," says Woodruff.
Since 1989, according to Alter, there's also been a decrease of hepatitis B among IV drug users. The drop "could be the result of education efforts and needle-exchange programs," she says, "but it's hard to believe that that could create such a large decline in that group." There has also been a modest decline in the number of heterosexual cases, Alter says, perhaps because more people are getting vaccinated.
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