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HIV is transmitted—that is, the virus enters the body—almost invariably by sexual contact, by blood-to-blood contact, or through pregnancy.

When HIV enters the body, it attaches itself only to certain sites on the walls of certain cells. The site on the cell wall is called the CD4 receptor, and the cell most commonly infected is called the CD4 cell. The CD4 cell is a white blood cell, or a lymphocyte. It belongs to a class of lymphocytes called T cells, which, along with B cells, are central parts of the immune system. (The CD4 cell is also called a T4 cell and a T-helper cell.) The CD4 cell’s job is to help coordinate the immune system’s defense against a variety of infectious diseases. HIV is carried by CD4 cells and other white blood cells to all parts of the body, including the brain. HIV also attaches itself to certain cells in the brain.

Once HIV attaches to a CD4 cell, it enters the cell. At this point, in a complicated series of events, the virus becomes part of the cell’s genes. Genes are composed of DNA, a molecule which is responsible for directing the reproduction of the cell. HIV is a virus and has only RNA, a molecule which is actually the mirror image of DNA but which cannot produce new viruses. HIV, however, is a retrovirus, meaning that it has a protein called reverse transcriptase. Reverse transcriptase allows the viral RNA to turn into a mirror image of itself; that is, it allows viral RNA to turn into viral DNA. This DNA then directs the infected cell to produce, not new CD4 cells, but new HIVs instead. The virus eventually destroys the CD4 cell, and the new viruses that have been produced then infect other CD4 cells. As CD4 cells are infected and destroyed, the immune system functions less and less effectively.

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In 1864, a Norwegian scientist reported that a patient developed diabetes after getting the mumps. Since then, more evidence has been found to link Type I diabetes with infectious diseases. Medical workers have noticed that diabetes in children, normally a rather rare disease (though it is growing ever more common), tends to occur in clusters. A number of cases will suddenly crop up in a particular area, and these outbreaks sometimes follow an epidemic of a viral disease, such as mumps or rubella (German measles). Coxsackie viruses (common viruses that can cause colds and intestinal infection) have also been implicated.

New cases of Type I diabetes seem to occur seasonally: most in the autumn and winter and least in the summer and spring—just like the incidence of many viral diseases. In some cases, diabetes “epidemics” follow virus epidemics closely; in others, there is a period of about three or four years between the outbreak of the viral disease and the appearance of diabetes symptoms.

Of course, it might be that the extra stress of the viral disease is just too much for a person who happens to have a weak pancreas, and the gland breaks down when the body is besieged by the disease germs. But researchers began to wonder whether the viral illness might actually damage the pancreas. Viruses might invade the pancreas and destroy the beta cells. Or there might be a more indirect effect, involving a mistaken attack by the body’s own defenses. The virus particles might happen to be chemically similar to part of the surface of the beta cells. (This kind of accidental similarity of environmental proteins to body biochemicals is called molecular mimicry.) Then antibodies produced by the body to attack the viruses would also attack and destroy beta cells. In any case, as beta cells are destroyed, the amount of insulin produced is greatly reduced. When 80 to 90 percent of the beta cells have been destroyed, the symptoms of diabetes develop quite suddenly.

There is a good deal of evidence to support the molecular mimicry theory. People with insulin-dependent diabetes usually make little or no insulin, and examinations of tissue from their pancreases show that beta cells have indeed been destroyed. Antibodies against these cells can be found circulating in the blood of a person with Type I diabetes. In fact, antibodies against one beta cell substance (glutamic acid decarboxylase, or GAD) may appear years before diabetes develops. Now researchers have confirmed that GAD is remarkably similar to a protein of the Coxsackie viruses.

All children catch viral diseases, usually quite a number of them during the growing years. Yet most children don’t develop diabetes. What determines that a virus infection will cause diabetes in one child, while another child will suffer the same infection and recover with full health?

If insulin-dependent diabetes is indeed an autoimmune disease—one in which the body makes antibodies against a virus that will also attack its own body cells—then a child who does not develop diabetes after a virus infection may just have been lucky enough not to produce those destructive antibodies. Each person produces his or her own unique antibodies against any particular germ or chemical. So some children may produce antibodies that simply cure them of the viral infection without affecting the pancreas.

Another possibility is that a person may inherit a pancreas or an immune system that is particularly susceptible to molecular mimicry. Researchers have found that most people with Type I diabetes have specific types of chemicals on the surfaces of their beta cells that are not usually found in other people. These cell-surface chemicals, which are hereditary, might be the chemicals against which a person’s body makes antibodies when viruses attack. (In Type II diabetes, this sort of correlation with special cell-surface chemicals is not seen.)

Although viruses may be implicated in Type I diabetes, this does not mean that diabetes is a contagious disease, like colds or mumps or TB. There is no “diabetes virus,” and you can’t catch diabetes by talking to, touching, or even kissing someone who has diabetes.

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Just a few years ago, cancer experts were enthusiastic about the strong possibility of soon canceling out breast cancer in women. The doctors had learned to use surgery and radiation treatment more precisely to attack the wildly growing cells. They also discovered how to shower the malignancy with strong anticancer drugs. They had new medications to protect healthy tissue from the bad effects of the drugs. Scientists also expected to rout out the cause of the disease, and with that knowledge they had hoped to cure breast cancer or to prevent it, or both.

But it has not happened – yet.

The American Cancer Society reports that, with 183,000 new cases annually, breast cancer kills 46,000 women each year. A woman, who lives to age 85, runs a one-in-nine chance of contracting breast cancer in her lifetime. Despite new therapies, the death rate has hardly changed in 50 years, and 70 percent of new cases are diagnosed in women who have no known risk factors for the disease.

That is dark news. Dr. Samuel Broder, director of the National Cancer Institute (NCI) in Bethesda, Maryland, maintains, “No question that we have a basis for optimism, but we should have no illusions about how difficult and formidable a problem breast cancer is. There won’t be a breakthrough tomorrow morning.”

Nobody knows that better than Dabney Allen, 49, a homemaker in MacLean, Virginia. Doctors first found a lump in a mammogram (a breast X-ray) of her right breast in 1990. “The biopsy showed that I had the kind of cancer that was 40 percent likely to recur,” Mrs. Allen tells Parade, “so I had both breasts removed.” After surgery, the doctors treated her with four potent drugs. “But the cancer recurred in March, under my right arm and along the scar,” Mrs. Allen says. “It spread to bone and to a spot on the chest wall. So my doctors say, ‘Let’s treat this as a chronic disease and not a terminal one.’”

Mrs. Allen will take drugs to kill her cancer cells. It is no cure, but she hopes by this method to alleviate the pain and stay comfortable for as long as possible.

The incidence of breast cancer increased by more than 30 percent from 1980 to 1987, prompting some to call the disease an epidemic. However, the American Cancer Society and the NCI believe the increase was due to more women having mammograms, which caught their cancer early. And Dr. Vincent DeVita, Jr., former head of the NCI, notes, “There is a definite decline in the death rate among young women with breast cancer.”

Still, Dr. Daniel Kopans, an associate professor of radiology at Harvard Medical School, believes that the number of new cases is increasing. Is there an epidemic? “Absolutely,” says Dr. Susan Love, director of University of California at Los Angeles’s Breast Center. “There are too many women dying of breast cancer, and we have to do something about it.”

What about mammograms? Dr. Kopans is angry with the NCI for its recent conclusion that women aged 40 to 49 do not benefit from annual mammograms. “If you screened all the women in the U.S. aged 40 to 49, you would save 3,000 lives a year,” Kopans estimates. The American Cancer Society and American Medical Association maintain that there is sufficient evidence to continue screening women in that age group.

However, several studies have shown that mammography screening provides little or no benefit for women under 50. Studies in the Netherlands, the United Kingdom, and Sweden, plus a Canadian study of 90,000 women, all showed that death rates from breast cancer for women in their 40s were the same whether or not they had screening mammograms.

“Mammography screening works great over 50,” says Dr. Love. “It has never really been proved to work that well in women under 50. The answer is: We need to find something that works better, not pay for something that doesn’t work as well.”

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