Current Trends Update: HIV-2 Infection -- United States

Human immunodeficiency virus type 2 (HIV-2) infection was first described in 1985 in asymptomatic West African prostitutes (1) and, in 1986, was reported in two West Africans with acquired immunodeficiency syndrome (AIDS) (2). The first confirmed case of HIV-2 infection in the United States was reported in late 1987 in a West African woman with AIDS (3). Since then, six additional cases of HIV-2 infection have been reported to CDC--three from Massachusetts, and one each from Connecticut, Rhode Island, and Florida. This article summarizes information about the six cases reported since 1987 (4-7).

Case 1. In May 1988, a 34-year-old woman developed fever, night sweats, head ache, and focal seizures. Evaluation, including an open brain biopsy, led to the diagnosis of cerebral toxoplasmosis. An enzyme immunoassay (EIA) for HIV-1 antibody and an HIV-1 Western blot (WB) assay were both negative, but an HIV-2-specific EIA and an HIV-2-specific WB were positive for HIV-2 antibody.

The woman, originally from West Africa, had married twice and had children from each marriage. Her first husband reportedly had many extramarital sex partners. She moved to the United States in the late 1970s; her second marriage was to an expatriate from her native country. She denied intravenous (IV)-drug use, extramarital sex partners, and receipt of transfusions. Her second husband and the four children who were tested had no serologic evidence of HIV-1 or HIV-2 infection.

Case 2. As part of the required medical screening process for immigration to the United States, a West African woman was tested for HIV infection in 1988 in Canada. The EIA for HIV-1 antibody was reactive, but the WB was indeterminate. Testing for HIV-2 antibody was positive by both HIV-2-specific EIA and HIV-2-specific WB. She had no history of AIDS or other HIV-related illnesses.

Before moving to the United States in 1984, the woman had had repeated sexual contact with a West African man who had had numerous female sex partners, including prostitutes. After moving to the United States, she married an expatriate from her native country. She denied IV-drug use, receipt of transfusions, and known occupational exposure to HIV-infected persons.

The woman was pregnant when HIV-2 antibody was detected, and she elected to terminate her pregnancy. Fetal tissue in poor condition was submitted for viral culture, but HIV-2 was not recovered. The woman had had a full-term stillborn infant in 1985 and a healthy infant in 1986. Her husband declined testing for himself and for their 2-year-old child.

Case 3. In August 1988, as part of ongoing unlinked testing of blood specimens from all newborn infants in Massachusetts, HIV-1 antibody was detected by EIA in a specimen, although HIV-1 WB was indeterminate. Because crossreactivity with HIV-2 was possible, the specimen was retested and found positive for HIV-2 by EIA and WB. The specimen was from a baby born in an inner-city Boston hospital. However, because of the unlinked survey, further testing and demographic characterization of the baby and HIV-2-infected mother are not possible.

Case 4. As part of the U.S. immigration process, a 45-year-old West African woman was tested for HIV in September 1988. She requested both an EIA and WB. The EIA was nonreactive, but the HIV-1 WB was positive. A subsequent EIA for HIV-2 antibody and an HIV-2-specific WB were both positive. The woman was in good health with no symptoms or signs of HIV-related illness.

The woman, who left West Africa in 1985, had been married to a native of her country who had no known risk factors for HIV infection. Her husband and their seven children, who remained in West Africa, were reported to be in good health. She married again within the year before her HIV-antibody test in 1988; HIV-1- and HIV-2-antibody tests were nonreactive for her second husband. She denied IV-drug use, history of transfusions, and occupational exposure to HIV.

Case 5. In January 1988, a 39-year-old West African man with a 3-month history of diarrhea and weight loss was diagnosed with Isospora belli infection. An HIV-1 antibody EIA was nonreactive. In August 1988, he was retested after the isosporiasis recurred, and had an indeterminate HIV-1 WB and positive HIV-2 WB. HIV-2-associated AIDS was con firmed by viral isolation; the man subsequently developed Candida esophagitis and Pneumocystis carinii pneumonia. He also has a chronic hepatitis B infection.

This man was born in West Africa and traveled throughout the world before moving to the United States in the early 1980s. His wife and four children remained in West Africa and are reportedly in good health but have not been tested for HIV. The man had multiple female sex partners in West Africa, southeast Asia, and the Caribbean but denied other risk behaviors for HIV infection.

Case 6. As part of the U.S. immigration process, a 32-year-old West African man was tested for HIV antibody. Initial EIA tests for HIV-1 antibody were reactive, but an HIV-1 WB was indeterminate. HIV-2-specific EIA and WB were positive. Although he had no history of HIV-associated illnesses, a tuberculin skin test and serologic tests for syphilis were positive; a chest radiograph showed no evidence of active tuberculosis.

In 1977, he was treated for a genital sore. In 1986, he had sexual contact with a woman from his country who had multiple sex partners. In late 1988, he entered the United States after living in Europe for 2 years. His wife and children remained in his native country and are in good health. He denied other risk behaviors for HIV infection.

Other cases. Five additional cases of HIV-2 infection are under investigation by the New York City Department of Health and another by the New York State Department of Health. Four of these persons are West Africans; the nationalities of the other two persons are unknown. Reported by: C Ruef, MD, P Dickey, MD, Yale Univ, New Haven; B Griffith, PhD, Veterans Administration Medical Center, West Haven, Connecticut. A Williams, PhD, C Fang, PhD, Transmissible Diseases Laboratory, Jerome H Holland Laboratories, American Red Cross, Rockville, Maryland. M Popovsky, MD, American Red Cross Blood Svcs--Northeast Region, Dedham; R D'Aquila, MD, Massachusetts General Hospital; J Ayanian, MD, J Maguire, MD, Brigham and Women's Hospital; R Marlink, MD, P Kanki, DVM, M Essex, DVM, Harvard School of Public Health, Boston; J Soares, MD, Sommerville Portugese American League, Sommerville; R Hoff, DSc, R Timperi, MPH, B Weiblen, MS, M Schwerzler, B Werner, PhD, GF Grady, MD, State Epidemiologist, Massachusetts Dept of Public Health. M Krieger, PhD, Genetic Systems Corp, Seattle, Washington. K Mayer, MD, Brown Univ, Providence; BA DeBuono, MD, State Epidemiologist, Rhode Island Dept of Health. S Beatrice, PhD, K Dressler, PhD, A Punsalang, PhD, R Stoneburner, MD, M Chiasson, PhD, New York City Dept of Health; P Smith, MD, R Stevens, PhD, J Wethers, MS, DL Morse, MD, State Epidemiologist, New York State Dept of Health. AIDS Program, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Infection with HIV-2 appears to be rare in the United States and is, largely or entirely, limited to imported cases. HIV-2 infection appears to be most prevalent in West Africa (8). Persons infected with HIV-2 have also been reported from Central Africa (9), Western Europe (8), Canada (5), and Brazil (10). In the United States (Table 1, page 579), all identified HIV-2-infected persons have been West Africans. All evidence suggests that these persons became infected through heterosexual contact with other infected West Africans. All but one of these cases of HIV-2 infection have been reported from northeastern states, reflecting, in part, the settlement pattern of West African expatriates in the United States. Because HIV-1 and HIV-2 are closely related, tests for antibody to one virus may crossreact with antibody to the other (11). Among Food and Drug Administration (FDA)-licensed tests, the sensitivity of HIV-1 EIAs for detecting HIV-2 antibody ranges from approximately 60% to greater than 90%, depending on the specific HIV-1 EIA employed and the clinical status of the infected person (12,13). When tested for antibody to HIV-1, persons infected with HIV-2 may be reactive by EIA but indeterminate or negative by WB (11). Therefore, confirmation of HIV-2 infection requires both HIV-1 and HIV-2 WB testing. Even when both tests are performed, however, HIV-2 may be difficult todifferentiate from HIV-1 infections (14). Assays for HIV-1- and HIV-2-specific peptides (15), the polymerase chain reaction procedure (16,17), or viral cultures (18) may be helpful in this situation.

HIV-2 infection should be considered in persons with clinical evidence of HIV infection who are HIV-1 EIA-nonreactive or who are HIV-1 EIA-reactive and HIV-1 WB-negative or -indeterminate. Persons from West Africa who have evidence of HIV infection should be evaluated for HIV-2 infection, regardless of HIV-1 EIA or WB results. HIV-2-specific EIAs and WBs have not yet been licensed by FDA. Testing is performed by CDC and other research laboratories.

Because the modes of transmission for HIV-2 and HIV-1 are likely to be the same, the recommended preventive measures are identical. CDC is monitoring the epidemiology of HIV-2 infection in the United States through case surveillance and serologic surveys of groups such as Peace Corps volunteers returning from Africa, sexually transmitted disease clinic patients, drug-treatment center patients, counseling and testing site clients, patients from sentinel hospitals, and potential blood donors.

Surveillance at blood collection agencies relies on the crossreactivity that exists between EIA tests for antibodies to HIV-1 and HIV-2. Among approximately 4 million potential U.S. blood donors per year, specimens reactive by HIV-1-specific EIA will be tested for HIV-2 infection with HIV-2-specific EIA and WB tests. However, few, if any, potential blood donors infected with HIV-2 are expected because FDA revised its recommendations to blood collection agencies in April 1988 to exclude donors who recently immigrated from sub-Saharan Africa or who are recent sexual contacts of West Africans (FDA, personal communication). None of the six HIV-2-infected persons reported here were actual or prospective blood donors.

From late 1986 to early 1988, CDC, FDA, and collaborating organizations tested greater than 22,000 serologic specimens, including greater than 10,000 specimens from persons at risk for HIV-1 infection, for serologic evidence of HIV-2 infection (3). Specimens were tested with HIV-1- and HIV-2-specific EIA, WB, and synthetic peptide tests. None of the specimens were positive for HIV-2 alone, although 10 specimens were reactive to both HIV-1- and HIV-2-specific synthetic peptides (Genetic Systems Corporation, unpublished data). These 10 persons might be infected with HIV-1 alone, HIV-2 alone, or both viruses. On the basis of this survey and the small number of known cases of HIV-2 infection, HIV-2 infection in the United States appears to be limited.

References

1. Barin F, M'Boup S, Denis F, et al. Serological evidence for virus

related to simian T-lymphotropic retrovirus III in residents of West Africa. Lancet 1985;2:1387-9.

2. Clavel F, Guetard D, Brun-Vezinet F, et al. Isolation of a new human retrovirus from West African patients with AIDS. Science 1986;233:343-6.

3. CDC. AIDS due to HIV-2 infection--New Jersey. MMWR 1987;37:33-5. 4. Ruef C, Dickey P, Schable CA, Griffith B, Williams AE, D'Aquila RT. A second case of the acquired immunodeficiency syndrome due to human immunodeficiency virus type 2 in the United States: the clinical implications. Am J Med 1989;86:709-12.

5. Neumann PW, O'Shaughnessy MV, Lepine D, D'Souza I, Mayor C, McLaughlin B. Laboratory diagnosis of the first cases of HIV-2 infection in Canada. Can Med Assoc J 1989;140:125-8.

6. Hoff R, Weiblen BJ, Schwerzler M, et al. Specific antibodies to HIV-2 detected in an anonymous newborn blood specimen from Massachusetts. Presented at the fourth Consensus Conference on Testing for Human Retroviruses. Kansas City, Missouri, March 7-9, 1989.

7. Ayanian JZ, Maguire JH, Marlink RG, Essex M, Kanki PJ. HIV-2 infection in the United States (Letter). N Engl J Med 1989;320:1422-3.

8. Horsburgh CR Jr, Holmberg SD. The global distribution of human immunodeficiency virus type 2 (HIV-2) infection. Transfusion 1988;28:192-5.

9. Georges AJ, Georges-Courbot MC, Salaun D, et al. Isolation of HIV-2 in Central Africa from AIDS patient and her symptom-free partner. Lancet 1988;1:188-9. 10. Veronesi R, Mazza CC, Santos Ferreira MO, Lourenco MH. HIV-2 in Brazil (Letter). Lancet 1987;2:402. 11. Clavel F. Editorial review: HIV-2, the West African AIDS virus. AIDS 1987;1:135-40. 12. George JR, Rayfield M, Schochetman G, et al. Sensitivity of U.S. FDA licensed HIV-1 enzyme immunoassays for detection of HIV-2 antibodies (Abstract). V International Conference on AIDS. Montreal, June 4-9, 1989:306. 13. Denis F, Leonard G, Sangare A, et al. Comparison of 10 enzyme immunoassays for detection of antibody to human immunodeficiency virus type 2 in West African sera. J Clin Microbiol 1988;26:1000-4. 14. Anonymous. HIV-2 in perspective (Editorial). Lancet 1988;1:1027-8. 15. Gnann JW Jr, McCormick JB, Mitchell S, Nelson JA, Oldstone MBA. Synthetic peptide immunoassay distinguishes HIV type 1 and HIV type 2 infections. Science 1987;237:1346-9. 16. Schochetman G, Ou C-Y, Jones WK. Polymerase chain reaction. J Infect Dis 1988;158:1154-7. 17. Rayfield M, De Cock K, Heyward W, et al. Mixed human immunodeficiency virus (HIV) infection in an individual: demonstration of both HIV type 1 and type 2 proviral sequences by using polymerase chain reaction. J Infect Dis 1988;158:1170-6. 18. Jackson JB, Balfour HH Jr. Practical diagnostic testing for human immunodeficiency virus. Clin Microbiol Rev 1988;1:124-38.

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