According to a report in the journal AIDS, one patient was infected by injecting drugs. His CD4 cell count fell from 680 in April 1999 to 240 in March 2001. The HIV in his blood was resistant to two of the three classes of anti-retroviral drugs available at the time.
In the second case, a man developed in January 2001 the flulike symptoms that are common immediately after HIV infection. He got the virus from sexual contact with a long-infected partner. By June, his CD4 count had fallen to 330, although it was back up to 510 in July. Steep CD4 declines followed by partial rebounds are common soon after infection; his case may have been an exaggerated version of that. His virus was also resistant to drugs in two classes of anti-retrovirals.
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Both men were eventually put on three- or four-drug combinations, Montaner said this week. The growth of HIV is fully suppressed, and there is no virus detectable now in either patient's bloodstream, which is the goal of treatment. In both cases, their drug combinations include drugs in the same class as medications that their virus was resistant to in lab tests.
The New York patient was started on anti-retroviral therapy two weeks ago, and it is too early to tell whether it is working.
In practice, many patients respond well to drug combinations that include medicines in classes to which they are resistant, in lab tests. In addition, resistance can sometimes be overcome by giving higher doses or several drugs from the same class.
Curiously, when someone who has developed drug resistance after years of treatment stops taking anti-retrovirals, the HIV in their blood often becomes susceptible to the same drugs again.
The dramatic downhill course the New York patient took could have meant that his HIV was especially virulent, but it could equally reflect preexisting weakness in his immune system that has nothing to do with the strain of virus.
"We know the whole progression to disease is multifactorial. It has to do with the patient, and it has to do with the virus. We don't know yet why some viruses cause rapid disease and some don't," said Miguel Quiñones-Mateu, a virologist at the Cleveland Clinic.
If tracing of the New York man's partners leads to many newly infected people who have also had very rapid progression of disease, however, that will tend to implicate the virus, not the hosts.
Tests on the New York man's virus show it has a trait known as "dual-tropism." When HIV invades a cell, it attaches to a CD4 receptor on the cell's surface and to a co-receptor, labeled R5 or X4. Most HIV strains attach to one or the other co-receptor. The New York virus can use both -- an unusual but not unique ability.