Important note: Information in this article was accurate in January 1988. The state of the art may have changed since the publication date.Morbidity and Mortality Weekly Report - January 29, 1988 / 37(3);33-5
Centers for Disease Control and Prevention
The first reported case of AIDS caused by human immunodeficiency virus type 2 (HIV-2) in the United States was diagnosed in December 1987. The patient, a West African, came to the United States in 1987. In December, the patient visited a physician because of a 3-year history of weight loss and recent onset of neurologic symptoms. A CAT scan of the head revealed mass lesions that biopsy showed to be caused by Toxoplasma gondii. Biopsy of a lymph node revealed acid-fast bacteria.
The patient did not give a history of sexual intercourse, use of nonsterile needles, or donation of blood while in the United States. All family members and household contacts, both in the United States and abroad, are reported to be well.
Because the diagnosis of cerebral toxoplasmosis without other underlying cause of immunodeficiency fits the CDC surveillance definition for AIDS, laboratory evidence of infection with HIV was sought. Testing of the patient's serum revealed a negative enzyme immunoassay (EIA) for antibody to HIV-1 with an indeterminate HIV-1 Western blot. However, EIA for antibodies to HIV-2 (Genetic Systems Corporation, Seattle, Washington (research test kit)) was repeatedly reactive and HIV-2 Western blot revealed bands for antibodies to gag (p26), pol (p34), and env (gp140) proteins. DNA amplification by the polymerase chain reaction technique with HIV-1- specific and HIV-2-specific DNA probes (1) revealed HIV-2 DNA but not HIV-1 DNA in the patient's lymphocytes and confirmed the diagnosis of HIV-2 infection. Reported by: SH Weiss, MD, J Lombardo, MD, PhD, J Michaels, MD, LR Sharer, MD, M Tayyarah, MD, J Leonard, MD, A Mangia, MD, P Kloser, MD, S Sathe, MD, R Kapila, MD, New Jersey Medical School, Univ of Medicine and Dentistry of New Jersey, Newark; NM Williams, MD, R Altman, MD, MPH, J French, MA, WE Parkin, DVM, State Epidemiologist, New Jersey State Dept of Health. Genetic Systems Corp, Seattle, Washington. AIDS Program, Center for Infectious Diseases, CDC.
Editorial Note: This patient represents the only documented case of HIV-2 infection in the United States. HIV-2 is closely related to HIV-1 and was first reported to be associated with AIDS in 1986 in West Africa, where the virus is believed to be endemic (2-8). Several well-documented cases of HIV-2 infection have also been reported among Europeans and among West Africans residing in Europe (3,4,8). The spectrum of disease and modes of transmission of HIV-2 are similar to those of HIV-1 (2-5). These modes of transmission include sexual intercourse; however, infected persons present no risk to nonsexual household contacts (9). The present case undoubtedly represents infection acquired in West Africa since illness began before the patients arrival in the United States. The patient has had no known activities that would have exposed others in this country to HIV-2.
Because of the reports of HIV-2 infection in West Africa and Europe, CDC and the Food and Drug Administration (FDA) initiated surveillance for HIV-2 in the United States in January 1987. To date, CDC, FDA, and collaborating investigators have screened 22,699 serum samples with anti-HIV-2 EIA (10). Of these specimens, 14,196 (63%) were from individuals whose activities placed them at increased risk for HIV-1 infection and who would, therefore, potentially be at risk for HIV-2 infection. The remaining 8,503 were from asymptomatic blood donors randomly selected from three areas of the United States, two of which have reported large numbers of AIDS patients. Overall, 35 (0.2%) of the serum samples were reactive by anti-HIV EIA using HIV-2 antigens but not by anti-HIV EIA using HIV-1 antigens. However, none of these EIAs could be confirmed when tested by HIV-2-specific Western blot. An additional 70 (0.3%) of the samples were reactive by Western blot with gag, pol, and env antigens of both HIV-1 and HIV-2. All of the dually reactive specimens were from individuals whose activities placed them at increased risk for HIV-1 infection. None were from the randomly selected blood donors. Sera from these dually reactive subjects were studied for the presence of type-specific neutralizing antibody to HIV-1 or HIV-2, antibody to synthetic peptides specific for HIV-1 or HIV-2 (Genetic Systems Corporation, Seattle, Washington (research test kit)), or HIV-1 and HIV-2 DNA by DNA amplification (1). Sixty of the subjects were shown to be infected with HIV-1 but not HIV-2. Ten are still under investigation.
It is reassuring that HIV-2-specific tests on sera from 22,699 persons, including 8,503 randomly selected U.S. blood donors, failed to reveal HIV-2 infection. However, the occasional presence of this virus in the United States, as in Europe, should be anticipated. The anti-HIV-1 EIA tests currently used for screening all U.S. blood donors are estimated to detect 42% to 92% of HIV-2 infections (4,11). Surveillance for HIV-2 in the United States is being continued to monitor the frequency of infection. Because the modes of transmission of HIV-1 and HIV-2 are similar, preventive measures for these related viruses are the same (12).
Ou C-Y, Kwok S, Mitchell SW, et al. DNA amplification for direct detection of HIV-1 in DNA of peripheral blood mononuclear cells. Science 1988 Jan 15;239(4837):295-7.
Clavel F, Guetard D, Brun-Vezinet F, et al. Isolation of a new human retrovirus from West African patients with AIDS. Science 1986 Jul 18;233(4761):343-6.
Brun-Vezinet F, Rey MA, Katlama C, et al. Lymphadenopathy-associated virus type 2 in AIDS and AIDS-related complex: clinical and virological features in four patients. Lancet 1987 Jan 17;1(8525):128-32.
Clavel F, Mansinho K, Chamaret S, et al. Human immunodeficiency virus type 2 infection associated with AIDS in West Africa. N Engl J Med 1987 May 7;316(19):1180-5.
Brun-Vezinet F, Rey MA, Dazza MC, et al. LAV-2/HIV-2 infection: clinical, epidemiological and virological features (Abstract no. THP.33). In: Abstracts of the third international conference on acquired immunodeficiency syndrome (AIDS). Washington, DC: US Department of Health and Human Services, Public Health Service, World Health Organization, 1987:169.
Antunes F, Odete Santos Ferreira M, Lourenco MH, Costa C, Pedro M. HIV infections in rural areas of West Africa (Guinea Bissau) (Abstract no. THP.88). In: Abstracts of the third international conference on acquired immunodeficiency syndrome (AIDS). Washington, DC: US Department of Health and Human Services, Public Health Service, World Health Organization, 1987:178.
Katlama C, Harzic M, Kourouma K, Dazza MC, Brun-Vezinet F. Seroepidemiological study of HIV1 and HIV2 infection in Guinea-Conakry (Abstract no. THP.75). In: Abstracts of the third international conference on acquired immunodeficiency syndrome (AIDS). Washington, DC: US Department of Health and Human Services, Public Health Service, World Health Organization, 1987:176.
Clavel F. HIV-2, the West African AIDS virus. AIDS 1987 Sep;1(3):135-40.
Friedland GH, Saltzman BR, Rogers MF, et al. Lack of transmission of HTLV-III/LAV infection to household contacts of patients with AIDS or AIDS-related complex with oral candidiasis. N Engl J Med 1986 Feb 6;314(6):344-9.
Schochetman G, Schable CA, Goldstein LC, Epstein J, Zuck TF. Screening of U.S. populations for the presence of LAV-II (Abstract no. THP.52). In: Abstracts of the third international conference on acquired immunodeficiency syndrome (AIDS). Washington, DC: US Department of Health and Human Services, Public Health Service, World Health Organization, 1987:172.
Denis F, Leonard G, Mounier M, et al. Efficacy of five enzyme immunoassays for antibody to HIV in detecting antibody to HTLV-IV. Lancet 1987 Feb 7;1(8528):324-5.
Public Health Service. Surgeon General's report on acquired immune deficiency syndrome. Washington, DC: US Department of Health and Human Services, Public Health Service, 1986.
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