Aids was first discovered when a group of individuals developed a cluster of symptoms indicative of:

Acute HIV infection (also known as seroconversion) is defined as the period between exposure to the virus and completion of the initial immune responses (when an antibody test becomes positive for HIV). After infection, HIV is able to replicate at an exponential rate using CD4 cells. See the image below.

Aids was first discovered when a group of individuals developed a cluster of symptoms indicative of:
Electron microscopy of human immunodeficiency virus (HIV)–1 virions. Courtesy of CDC/Dr. Edwin P. Ewing, Jr.

The following is a simplified outline of events that occur during acute HIV infection. [2]

On day 0, the individual is exposed to HIV, and infection begins.

On about day 8, the virus is detectable in blood using antigen tests such as polymerase chain reaction (PCR); however, antibody test findings are negative. The amount of virus in the blood more than doubles every day. The CD4 cell count (and total white blood cell count) begins to drop as the viral load increases.

During weeks 2-4, early antibodies to HIV may be detected; however, they have a low affinity for viral antigens and have little effect on the virus itself. Newer antibody assays may detect these antibodies. The viral load peaks and begins to decline as the immune system begins to battle the virus with antibodies and CD8 cytotoxic cells.

Although persons infected with HIV may transmit the infection to another person at any time, they are highly infectious during the period of acute infection when genital shedding of HIV virus peaks, which occurs at approximately week 3-4 of acute infection. The individual may be asymptomatic during this period and thus may have no knowledge that he or she is infected and so may not use appropriate safer-sex precautions. This represents an epidemiologic challenge in controlling the HIV pandemic.

During weeks 10-24, the HIV viral load drops to its lowest point, also known as the set point, which is different in each person. Antibodies now have higher affinity for viral antigen; therefore, antibody tests become positive for HIV. Seroconversion is now complete, and chronic HIV infection begins.

Persistent generalized lymphadenopathy

This is often the earliest symptom of primary HIV infection. Because of marked follicular hyperplasia in response to HIV infection, the lymph nodes have very high viral concentrations. Persistent generalized lymphadenopathy may be observed at any point in the spectrum of immune dysfunction and is not associated with an increased likelihood of developing AIDS.

Oral lesions

Thrush can result from Candida infection; oral hairy leukoplakia is presumably due to Epstein-Barr virus (EBV) infection. Thrush is usually a sign of fairly advanced immunologic decline, generally occurring in individuals with CD4 cell counts of 200-500/µL.

HSV lesions can also reflect deteriorating immune function in patients infected with HIV. Aphthous ulcers of the posterior oropharynx affect 10-20% of patients infected with HIV. Their etiology is unknown. These ulcers can be very painful and can cause dysphagia if left untreated.

Hematologic disturbances

Upon disease progression, individuals with HIV infection develop a moderate to severe hypoproliferative anemia. The most common form of anemia observed in patients infected with HIV has the characteristics of anemia of chronic disease. In addition, anemia may be a complication of opportunistic infections or may be due to marrow damage from the virus or from antiretroviral drug toxicity (eg, zidovudine).

Thrombocytopenia may be an early manifestation of HIV infection. Approximately 3% of patients infected with HIV with CD4 cell counts greater than 400/µL have platelet counts of less than 150,000/µL. Of patients who have CD4 cell counts less than 400 cells/µL, 10% also have platelet counts of less than 150,000 cells/µL.

HIV-associated thrombocytopenia is rarely a serious clinical problem. In most cases, platelet counts remain greater than 50,000 cells/µL and the condition can be treated conservatively.

Idiopathic thrombocytopenia in persons with HIV infection is very similar to the thrombocytopenia observed in individuals with idiopathic thrombocytopenic purpura (ITP). Antibodies against HIV (anti-GP160/120) have been shown to also bind to platelets (anti-GPIIb/IIIa). [3] Because these data point to an immunologic basis for thrombocytopenia in persons infected with HIV, most of the treatments used are immune-based.

Another mechanism for HIV-induced thrombocytopenia is a direct effect of HIV on megakaryocytes. This is evidenced by a defect and subsequent decrease in platelet production.

In addition, thrombocytopenia has been reported as a consequence of classic thrombotic thrombocytopenic purpura (TTP) in patients infected with HIV. This clinical syndrome, consisting of fever, thrombocytopenia, hemolytic anemia, and neurologic and renal dysfunction, is a rare complication of early HIV infection.

Neurologic disorders

Aseptic meningitis can be observed in all but the very late stages of HIV infection. This suggests that aseptic meningitis in the setting of HIV infection is an immune-mediated disease. Aseptic meningitis due to HIV infection usually resolves spontaneously within 2-4 weeks. Signs and symptoms may persist long-term in some patients.

Through unknown mechanisms, HIV infection can mimic Guillain-Barré syndrome (acute inflammatory demyelinating polyradiculoneuropathy).

Mononeuritis multiplex, a necrotizing arteritis of peripheral nerves, is another autoimmune peripheral neuropathy observed in patients infected with HIV.

Zidovudine can cause myopathy; this is often reversible once the drug is discontinued. HIV infection can also cause myopathy by direct damage to the muscle cells. The exact mechanism has not yet been elucidated.

Dermatologic conditions

Reactivation of varicella-zoster virus (shingles) occurs in 10-20% of patients infected with HIV. Onset of shingles indicates a modest decline in immune function and is often the first clinical indication of immunodeficiency.

In the tortuous mythology of the AIDS epidemic, one legend never seems to die: Patient Zero, a.k.a. Gaétan Dugas, a globe-trotting, sexually insatiable French Canadian flight attendant who supposedly picked up H.I.V. in Haiti or Africa and spread it to dozens, even hundreds, of men before his death in 1984.

Mr. Dugas was once blamed for setting off the entire American AIDS epidemic, which traumatized the nation in the 1980s and has since killed more than 500,000 Americans. The New York Post even described him with the headline “The Man Who Gave Us AIDS.”

But after a new genetic analysis of stored blood samples, bolstered by some intriguing historical detective work, scientists on Wednesday declared him innocent.

The strain of H.I.V. responsible for almost all AIDS cases in the United States, which was carried from Zaire to Haiti around 1967, spread from there to New York City around 1971, researchers concluded in the journal Nature. From New York, it spread to San Francisco around 1976.

The new analysis shows that Mr. Dugas’s blood, sampled in 1983, contained a viral strain already infecting men in New York before he began visiting gay bars in the city after being hired by Air Canada in 1974.

The researchers also reported that originally, Mr. Dugas was not even called Patient Zero — in an early epidemiological study of cases, he was designated Patient O, for “outside Southern California,” where the study began. The ambiguous circular symbol on a chart was later read as a zero, stoking the notion that blame for the epidemic could be placed on one man.

Myths like that of Patient Zero echo in prevention efforts even today, experts said. Many vulnerable groups, including young gay men and African women, fail to use protective drugs or avoid testing because they fear being stigmatized or accused of being carriers.

Reflecting on the epidemic’s early days, Dr. Anthony S. Fauci, then a doctor treating AIDS patients and now the director of the National Institute of Allergy and Infectious Diseases, said he remembered it seeming plausible at the time that one person was responsible.

In hindsight, he added, the idea now seems absurd. “We were unaware of how widespread it was in Africa,” Dr. Fauci said. “Also, we thought, based on very little data, that it was only about two years from infection to death.”

The new data is consistent with the scenario described in 2011 in “The Origins of AIDS,” by Dr. Jacques Pépin, an infectious disease specialist at the University of Sherbrooke in Quebec.

Relying on previous genetic research and African colonial records, Dr. Pépin showed that H.I.V. was carried from Kinshasa to Haiti in the 1960s — most likely by one of the thousands of Haitian civil servants recruited by the United Nations to work in the former Belgian Congo after colonial rule collapsed.

Gaétan Dugas, the flight attendant once described as Patient Zero in the American AIDS epidemic.

In Haiti, he theorized, a few cases were multiplied by unsterile conditions at a private blood-collecting company, Hemo-Caribbean, that opened in 1971 and exported 1,600 gallons of plasma to the United States monthly. Plasma clotting factors were used by American hemophiliacs, many of whom died of AIDS.

Haiti was also a sex-tourism destination for gay men, another route the virus could have taken to New York.

The blood samples analyzed in the new study were collected in 1978 and 1979 in New York City and San Francisco as part of an effort to make a hepatitis B vaccine. Researchers stored almost 16,000 blood samples; nearly 7 percent of those from New York and 4 percent of those from California later turned out to be infected with H.I.V.

A team led by Michael Worobey, an evolutionary biologist at the University of Arizona in Tucson and the lead author of the Nature paper, sequenced the genomes of the H.I.V. found in some of those samples and compared them with viral DNA in samples collected in the early 1980s from Haitians, Dominicans and others treated in American hospitals.

Because decades spent in freezers had degraded many samples, Dr. Worobey said, his lab developed an “RNA jackhammering” technique similar to that used to reconstruct the ancient Neanderthal genome. Counting mutations allowed the researchers to “wind back the molecular clock” and see when each strain of H.I.V. diverged from its ancestors.

Africa has a dozen H.I.V. groups, and Haiti’s epidemic came from one of those. The New York samples all derive from one Haitian strain, and those from San Francisco are all so closely related that they probably all resulted from one person introducing one New York strain, Dr. Worobey said.

Thomas Ramos, an AIDS patient, at a hospital in New York, in July 1987. The epidemic has killed more than 500,000 Americans.Credit...Alon Reininger/Contact Press Images

The symptoms that were later called AIDS were first recognized in 1981, and the legend of Patient Zero began with a 1984 study that traced the sexual contacts of 40 gay men with Kaposi’s sarcoma or other indicators of late-stage AIDS. Eight of them, half in New York and half in Southern California, had had sex with an unidentified flight attendant.

Initially described as “Case 057” and then as Patient O, he reported having about 250 sexual partners a year.

That study incorrectly assumed that most patients developed AIDS symptoms within about 10 months of infection. In reality, it takes years — so some participants may have been infected long before meeting Mr. Dugas.

Also, Mr. Dugas may have become the cluster’s focal point partly because he kept a diary. Men in the study reported an average of 227 partners a year, often quick, anonymous encounters in bars and bathhouses.

But Mr. Dugas gave investigators 72 names.

Dr. Harold W. Jaffe, who was one of the original investigators and is now the associate director for science at the Centers for Disease Control and Prevention, said the text of the original article referred to a “patient outside California.”

But the chart, of which he had an early copy, was admittedly ambiguous. At the center is the “O” or “0,” identified as the “index patient.” The other cases are numbered: “LA3” and “NY15,” for example.

Young men with AIDS walking in San Francisco in 1986.Credit...Alon Reininger/Contact Press Images

The legend itself sprang from the publicity campaign for a best-selling 1987 book, “And the Band Played On,” by Randy Shilts, a gay San Francisco journalist who himself died of AIDS in 1994.

In a 1993 interview, Mr. Shilts said he had heard C.D.C. investigators use the term Patient Zero and thought, “Oooh, that’s catchy.”

By hunting down former boyfriends of men in the 1984 study, Mr. Shilts established that the flight attendant was Mr. Dugas, who was born in Quebec but lived his last years in Vancouver, British Columbia.

Mr. Shilts said he was initially horrified that his publisher, St. Martin’s Press, focused his book tour on Patient Zero instead of the government’s slow response to the epidemic, but he went along.

Although Mr. Shilts did not accuse Mr. Dugas of starting the American epidemic, he demonized him as a deliberate spreader of the virus who ignored a doctor’s demand that he stop having unprotected sex, and coldbloodedly told some sex partners that he had “gay cancer” and now they might get it.

Back in 1984, the term Patient Zero was not normally used to describe an outbreak’s first case, said Dr. Jaffe, an author of the new Nature paper. “I don’t remember who first used it,” he said. “But after Randy Shilts did, we started saying it ourselves.”

Marchers called attention to the growing AIDS epidemic in New York City in June 1983.Credit...Alon Reininger/Contact Press Images

Later, he said, when reporters asked if Mr. Dugas had brought AIDS to North America, “We said no, that he wasn’t the first.”

Dr. Jaffe added: “But I think they went with it anyway. The idea of Patient Zero was very attractive. Letter O would not be a story.”

Richard A. McKay, a Cambridge historian and another author of the Nature paper, has long fought for Mr. Dugas’s reputation, saying his friends in Vancouver’s gay community had painted a sympathetic portrait of him for Mr. Shilts, who ignored it.

Humanizing Mr. Dugas could help in the fight to end the epidemic, said Dr. Robert M. Grant, an AIDS researcher at the University of California, San Francisco.

Even though the disease can now be prevented and controlled, many people — in San Francisco and in Africa, he said — resist getting tested for H.I.V. and fool themselves into believing they are not at risk because they fear being blamed by their social circle.

“No one wants to be the Patient Zero of their village,” he said. “But this may be helpful because it says, ‘Just because you are the first to be diagnosed doesn’t mean you started the epidemic.’”