Why June 5?
June 5, 1981, is the beginning of AIDS Awareness before it was identified as AIDS. It is an important day in the history of HIV/AIDS. HIV Long-Term Survivors Awareness Day is June 5, 2019. It is the 38th anniversary of the day AIDS arrived unannounced, unnamed and unwelcome in our lives via a report by the U.S. Centers for Disease Control and Prevention (CDC) in the Morbidity and Mortality Weekly Report (MMRW)
It described five cases of Pneumocystis carinii pneumonia (PCP) among five previously healthy young gay men in Los Angeles. Two of them had already died. It’s the first official reporting of the AIDS epidemic. It was the earthquake that shook that eventually shook the planet.
June 5, 1981 is cited as the beginning of the AIDS pandemic.
Today we know that HIV doesn’t discriminate and impacts people of all ages, races, sexual orientations, and socio-economic backgrounds. Currently 26% of all 1.4 million people living with HIV in the U.S. became positive before 1996, meaning they are long-term survivors.
HIV Long-Term Survivors Awareness Day is was created in 2014 by Tez Anderson, a thirty-six-year long survivor and founder of Let’s Kick ASS—AIDS Survivor Syndrome, the lead sponsor of the day.
Currently 26% of all 1.3 million people living with HIV in the U.S. are HIV Long-Term Survivors.
We celebrate those who have defied the odds by living with HIV for decades.
June 5 is about coming together and realizing that we are not alone. It is a national day of storytelling. We want to collect the stories of our lives, resilience, and our survival.
With courage and compassion, we survived the darkest days of the plague. Without access to effective treatments, we were forced to rely on each other and ourselves. As individuals and community, we exhibited strength we didn’t know we had. Now we face the conundrums of aging with HIV.
HIV Long-Term Survivors Awareness day is about celebrating our survival and looking forward to envisioning and create the lives we never imagined we’d live.
We want to change the narrative from survival to thriving and Healthy Aging with HIV. Long-term survival, once an almost unimaginable concept is now the norm — something that was unimaginable before 1996.
Today 60% of all people living with HIV in the US are over 50. By 2020 that will increase to 70 percent. Aging is the new face of HIV. Yet it feels as though the HIV global Our focus is on ensuring that HIV Long-Term Survivors are front and center in the current HIV dialogue.
HIV and Aging are not a monolith. Pre-HAART survivors and Post-HAART survivors constitute separate cohorts with overlapping but different medical and psychosocial needs. Longest term survivors face unique social and mental health challenges as well as medical issues none of us ever imagined.
We’re the generation who were told to plan to die young. By the end of that year, in the U.S. we witnessed the deaths of 362,004 of our loved ones and community. 6.4 million people had died from AIDS worldwide.
There’s a meme that “we lost an entire generation.” While we did a lot of our generation there are by recent estimates, 26% of Longest-Term Survivors alive now.
Let’s celebrate, honor and appreciate that they still have years go and it is all our job to help them become the best they can be.
In the first days of this new pestilence, it quickly became known as Gay Cancer. Then it became GRID, for gay-related immunodeficiency and A.I.D., for acquired immunodeficiency disease. It would later be identified as HIV/AIDS. Today we are aware that HIV doesn’t discriminate and impacts people of all ages, races, sexual orientations, and socio-economic backgrounds.
Remembering the Early Days of 'Gay Cancer'
Commentator Joe Wright spent more than 10 years doing AIDS community work in San Francisco. He says that back in 1981…
On June 5, 1981, MMWR published a report of five cases of Pneumocystis carinii pneumonia (PCP) among previously healthy young men in Los Angeles (1). All of the men were described as “homosexuals”; two had died. Local clinicians and the Epidemic Intelligence Service (EIS) Officer stationed at the Los Angeles County Department of Public Health, prepared the report and submitted it for MMWR publication in early May 1981. Before publication, MMWR editorial staff sent the submission to CDC experts in parasitic and sexually transmitted diseases. The editorial note that accompanied the published report stated that the case histories suggested a “cellular-immune dysfunction related to a common exposure” and a “disease acquired through sexual contact.” The report prompted additional case reports from New York City, San Francisco, and other cities. At about the same time, CDC’s investigation drug unit, the sole distributor of pentamidine, the therapy for PCP, began to receive requests for the drug from physicians also to treat young men. In June 1981, CDC developed an investigative team to identify risk factors and to develop a case definition for national surveillance. Within 18 months, epidemiologists conducted studies and prepared MMWR reports that identified all of the major risks factors for acquired immnodeficiency syndrome (AIDS). In March 1983, CDC issued recommendations for prevention of sexual, drug-related, and occupational transmission based on these early epidemiologic studies and before the cause of the new, unexplained illness was known.
Complete text of MMRW report issued June 5, 1981
Epidemiologic Notes and Reports
Pneumocystis Pneumonia — Los Angeles
In the period October 1980-May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3 different hospitals in Los Angeles, California. Two of the patients died. All 5 patients had laboratory-confirmed previous or current cytomegalovirus (CMV) infection and candidal mucosal infection. Case reports of these patients follow.
Patient 1: A previously healthy 33-year-old man developed P. carinii pneumonia and oral mucosal candidiasis in March 1981 after a 2-month history of fever associated with elevated liver enzymes, leukopenia, and CMV viruria. The serum complement-fixation CMV titer in October 1980 was 256; in may 1981 it was 32.* The patient’s condition deteriorated despite courses of treatment with trimethoprim-sulfamethoxazole (TMP/SMX), pentamidine, and acyclovir. He died May 3, and postmortem examination showed residual P. carinii and CMV pneumonia, but no evidence of neoplasia.
Patient 2: A previously healthy 30-year-old man developed p. carinii pneumonia in April 1981 after a 5-month history of fever each day and of elevated liver-function tests, CMV viruria, and documented seroconversion to CMV, i.e., an acute-phase titer of 16 and a convalescent-phase titer of 28* in anticomplement immunofluorescence tests. Other features of his illness included leukopenia and mucosal candidiasis. His pneumonia responded to a course of intravenous TMP/.SMX, but, as of the latest reports, he continues to have a fever each day.
Patient 3: A 30-year-old man was well until January 1981 when he developed esophageal and oral candidiasis that responded to Amphotericin B treatment. He was hospitalized in February 1981 for P. carinii pneumonia that responded to TMP/SMX. His esophageal candidiasis recurred after the pneumonia was diagnosed, and he was again given Amphotericin B. The CMV complement-fixation titer in March 1981 was 8. Material from an esophageal biopsy was positive for CMV.
Patient 4: A 29-year-old man developed P. carinii pneumonia in February 1981. He had had Hodgkins disease 3 years earlier, but had been successfully treated with radiation therapy alone. He did not improve after being given intravenous TMP/SMX and corticosteroids and died in March. Postmortem examination showed no evidence of Hodgkins disease, but P. carinii and CMV were found in lung tissue.
Patient 5: A previously healthy 36-year-old man with clinically diagnosed CMV infection in September 1980 was seen in April 1981 because of a 4-month history of fever, dyspnea, and cough. On admission he was found to have P. carinii pneumonia, oral candidiasis, and CMV retinitis. A complement-fixation CMV titer in April 1981 was 128. The patient has been treated with 2 short courses of TMP/SMX that have been limited because of a sulfa-induced neutropenia. He is being treated for candidiasis with topical nystatin.
The diagnosis of Pneumocystis pneumonia was confirmed for all 5 patients antemortem by closed or open lung biopsy. The patients did not know each other and had no known common contacts or knowledge of sexual partners who had had similar illnesses. Two of the 5 reported having frequent homosexual contacts with various partners. All 5 reported using inhalant drugs, and 1 reported parenteral drug abuse. Three patients had profoundly depressed in vitro proliferative responses to mitogens and antigens. Lymphocyte studies were not performed on the other 2 patients.
Reported by MS Gottlieb, MD, HM Schanker, MD, PT Fan, MD, A Saxon, MD, JD Weisman, DO, Div of Clinical Immunology-Allergy; Dept of Medicine, UCLA School of Medicine; I Pozalski, MD, Cedars-Mt. Siani Hospital, Los Angeles; Field services Div, Epidemiology Program Office, CDC.
Editorial Note: Pneumocystis pneumonia in the United States is almost exclusively limited to severely immunosuppressed patients (1). The occurrence of pneumocystosis in these 5 previously healthy individuals without a clinically apparent underlying immunodeficiency is unusual. The fact that these patients were all homosexuals suggests an association between some aspect of a homosexual lifestyle or disease acquired through sexual contact and Pneumocystis pneumonia in this population. All 5 patients described in this report had laboratory-confirmed CMV disease or virus shedding within 5 months of the diagnosis of Pneumocystis pneumonia. CMV infection has been shown to induce transient abnormalities of in vitrocellular-immune function in otherwise healthy human hosts (2,3). Although all 3 patients tested had abnormal cellular-immune function, no definitive conclusion regarding the role of CMV infection in these 5 cases can be reached because of the lack of published data on cellular-immune function in healthy homosexual males with and without CMV antibody. In 1 report, 7 (3.6%) of 194 patients with pneumocystosis also had CMV infection’ 40 (21%) of the same group had at least 1 other major concurrent infection (1). A high prevalence of CMV infections among homosexual males was recently reported: 179 (94%) had CMV viruria; rates for 101 controls of similar age who were reported to be exclusively heterosexual were 54% for seropositivity and zero fro viruria (4). In another study of 64 males, 4 (6.3%) had positive tests for CMV in semen, but none had CMV recovered from urine. Two of the 4 reported recent homosexual contacts. These findings suggest not only that virus shedding may be more readily detected in seminal fluid than urine, but also that seminal fluid may be an important vehicle of CMV transmission (5).
All the above observations suggest the possibility of a cellular-immune dysfunction related to a common exposure that predisposes individuals to opportunistic infections such as pneumocystosis and candidiasis. Although the role of CMV infection in the pathogenesis of pneumocystosis remains unknown, the possibility of P. carinii infection must be carefully considered in a differential diagnosis for previously healthy homosexual males with dyspnea and pneumonia.
- Walzer PD, Perl DP, Krogstad DJ, Rawson G, Schultz MG. Pneumocystis carinii pneumonia in the United States. Epidemiologic, diagnostic, and clinical features. Ann Intern Med 1974;80:83–93.
- Rinaldo CR, Jr, Black PH, Hirsh MS. Interaction of cytomegalovirus with leukocytes from patients with mononucleosis due to cytomegalovirus. J Infect Dis 1977;136:667–78.
- Rinaldo CR, Jr, Carney WP, Richter BS, Black PH, Hirsh MS. Mechanisms of immunosuppression in cytomegaloviral mononucleosis. J Infect Dis 1980;141:488–95.
- Drew WL, Mintz L, Miner RC, Sands M, Ketterer B. Prevalence of cytomegalovirus infection in homosexual men. J Infect Dis 1981;143:188–92.
- Lang DJ, Kummer JF. Cytomegalovirus in semen: observations in selected populations,. J Infect Dis 1975; 132:472–3.