Seronegative HIV-1 infection appears to be caused by an inability of the host to form HIV-1-specific antibodies, rather than to a highly virulent strain of the virus as has been suggested in the past, investigators in Portugal report.

Dr. Ana R. Cardoso, at Hospital Nossa Senhora da Craca in Tomar, and associates treated a woman who presented in 2001 with fever, malaise, anorexia and oral thrush. Serological testing in 1997 and 1999 had yielded negative results, as were those performed in October, November and December.

The diagnosis was made in December based on the detection of p24 antigen and HIV-1 RNA in plasma, the authors report in the April 30th issue of AIDS. Her current sexual partner was tested and found to be seropositive, even though he was asymptomatic.

Dr. Cardoso’s group sequenced regions of the env and gag genes from both individuals.

Both were infected with HIV-1 subsubtype A2. That from the man had more sequence divergence, whereas that from the woman had very low genetic diversity, “consistent with a recent infection and the absence of immunologic pressure imposed on the viruses.”

“Further studies are needed to permit the identification of the immunological defect causing seronegative HIV-1 infection, because this may have important implications for diagnosis, the prevention of viral transmission and vaccination,” they conclude.

Washington Post Staff Writer
Wednesday, November 26, 2008; Page A04

A strategy of testing adults every year for HIV and immediately treating every person found to be infected could virtually end the AIDS epidemic in Africa in about a decade, new research suggests.

While nobody is seriously espousing that approach, the “thought experiment” outlined this week in the Lancet journal emphasizes the usefulness of antiretroviral drugs as tools for preventing the spread of HIV infection as well as treating it.

The power of AIDS drugs to dramatically slow the epidemic is the consequence of two well-established facts.

The first is that the amount of virus circulating in the bloodstream is the most important factor determining whether an infected person transmits the disease to another during a high-risk encounter. The second is that AIDS drugs can lower this “viral load” in the bloodstream to one-millionth of what it is without treatment.

BERLIN (Reuters) – A bone marrow transplant using stem cells from a donor with natural genetic resistance to the AIDS virus has left an HIV patient free of infection for nearly two years, German researchers.

The patient, an American living in Berlin, was infected with the human immunodeficiency virus that causes AIDS and also had leukemia. The best treatment for the leukemia was a bone marrow transplant, which takes the stem cells from a healthy donor’s immune system to replace the patient’s cancer-ridden cells.

Dr. Gero Hutter and Thomas Schneider of the Clinic for Gastroenterology, Infections and Rheumatology of the Berlin Charite hospital said on Wednesday the team sought a bone marrow donor who had a genetic mutation known to help the body resist AIDS infection.

The mutation affects a receptor, a cellular doorway, called CCR5 that the AIDS virus uses to get into the cells it infects.

When they found a donor with the mutation, they used that bone marrow to treat the patient. Not only did the leukemia disappear, but so did the HIV.

“As of today, more than 20 months after the successful transplant, no HIV can be detected in the patient,” the clinic said in a statement.

“We performed all tests, not only with blood but also with other reservoirs,” Schneider told a news conference.

“But we cannot exclude the possibility that it’s still there.”

The researchers stressed that this would never become a standard treatment for HIV. Bone marrow stem cell transplants are rigorous and dangerous and require the patient to first have his or her own bone marrow completely destroyed.

Patients risk death from even the most minor infections because they have no immune system until the stem cells can grow and replace their own.

HIV has no cure and is always fatal. Cocktails of drugs can keep the virus suppressed, sometimes to undetectable levels. But research shows the virus never disappears — it lurks in so-called reservoirs throughout the body.

Hutter’s team said they have been unable to find any trace of the virus in their 42-year-old patient, who remains unnamed, but that does not mean it is not there.

“The virus is tricky. It can always return,” Hutter said.

The CCR5 mutation is found in about 3 percent of Europeans, the researchers said. They said the study suggests that gene therapy, a highly experimental technology, might someday be used to help treat patients with HIV.

(Reporting by Oliver Denzer; Writing by Maggie Fox in Washington; Editing by Vicki Allen)