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Seroconversion to Simian Immunodeficiency Virus in Two Laboratory Workers

Simian immunodeficiency viruses (SIVs) are lentiviruses that cause acquired immunodeficiency syndrome (AIDS)-like illnesses in susceptible macaque monkeys and are used in the study of AIDS (1). In November 1988, CDC published guidelines to minimize the risk of SIV transmission to research laboratory workers (2). This report summarizes the investigation of two laboratory workers who seroconverted following occupational exposures to SIV. Case 1

In March 1990, a technician at a research laboratory sustained a stick with a blood-contaminated needle while attempting to disconnect the vacutainer holder from the needle after obtaining blood from an anesthetized SIV-infected macaque. The macaque had been inoculated with SIV 6 months earlier, had seroconverted, was SIV culture-positive, and was symptomatic. The needle, visibly contaminated with blood, penetrated a latex glove and produced a deep puncture wound that caused the thumb to bleed. After removing the glove, the worker immediately scrubbed the wound with a povidone-iodine solution and then with a 10% bleach solution. Marked inflammation and swelling developed at the wound site and persisted for several weeks. The worker was treated with oral dicloxacillin and warm compresses. The wound site was not cultured.

Serum samples collected 1 week before the exposure, 1 week after the exposure, monthly over the following 12 months, and 19 months later were tested. None were reactive to human immunodeficiency virus (HIV)-1 by enzyme immunoassay (EIA) or by Western blot (WB) or to HIV-2 or SIV by whole-virus EIAs. However, serum samples obtained during June 1990-March 1991 were reactive to a number of synthetic peptides derived from the transmembrane region of SIV and HIV-2, and the titer to one of these peptides peaked from June through August 1990, and subsequently declined.

Testing by HIV-2 WB first showed reactivity to envelope (env) gp41 from a sample obtained during July 1990; testing showed a weak reactivity to group-specific antigen (gag) p27 in all the samples, including the preexposure sample. SIV WB showed no bands on the serum samples obtained during March-June 1990 and a weak gag p27 band after July 1990. Radioimmunoprecipitation (RIPA) also showed reactivity to the env protein gp130 in serum samples obtained during August 1990-March 1991, with peak intensity in the sample obtained in August (3).

Cultures of peripheral blood mononuclear cells (PBMCs) collected monthly were negative for SIV. Polymerase chain amplification (PCR) of PBMCs using primers and probes from the gag (4) and polymerase (pol) (5) region of SIV with nested amplification in pol, and with pol-, LTR- and env-nested primers representing consensus sequences of HIV-2 and SIV (5) were also negative (3).

Thirteen months after the exposure, 10 mL of heparinized blood obtained from the worker was inoculated into a young, healthy, SIV-negative Rhesus macaque. For 10 months after inoculation, biweekly to monthly serum samples obtained from the monkey were negative for SIV antibody by whole-virus EIA and by synthetic peptide EIAs, and the monkey showed no evidence of SIV infection by PCR. Case 2

A laboratory worker at another research facility, first tested in April 1992, was reactive by HIV-2 whole-virus and peptide EIAs and by SIV-peptide EIA and negative by HIV-1 EIA and WB. HIV-2 WB showed reactivity to numerous viral proteins including gag, pol, and env.

The worker had no history of percutaneous or mucous membrane exposure to SIV. However, during September-October 1989, the worker had severe dermatitis involving the forearms and hands that required treatment with oral steroids. The worker performed serology on clinical specimens from SIV-infected monkeys without gloves. The person also worked with SIV-infected cell cultures, but all procedures were done in a laminar flow biosafety cabinet with protective wear (laboratory coat and gloves).

Serum samples from the laboratory worker obtained during 1988 and one during November 1989 were thawed and tested and were negative for HIV-1, HIV-2, and SIV seroreactivity by EIA and WB. A stored serum sample from the worker obtained during April 1990 was reactive by HIV-2 and SIV EIA, and showed gag and env reactivity by HIV-2 WB. Testing of nine other serum specimens obtained from the worker during April 1990-April 1992 showed persistent seroreactivity to HIV-2 and SIV. Serum titers to one peptide derived from the transmembrane region of HIV-2 showed an increase in titer over this 2-year period. PCR amplification and viral cultures of PBMCs are pending. Additional Information

Neither of the two workers have any risk factors for HIV-1 or HIV-2 infection. Both have been in long-term, monogamous sexual relationships, and their respective sex partners tested seronegative for HIV and SIV by EIA and WB. Neither of the two workers had any illness suggestive of an acute retroviral infection and both remain well, with no clinical or laboratory evidence of immunodeficiency. Reported by: Retrovirus Diseases Br, Div of Viral and Rickettsial Diseases, and Laboratory Investigations Br, Div of HIV/AIDS, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: SIVs are primate lentiviruses morphologically similar and biologically related to HIV-1 and HIV-2 (6,7). These viruses share with HIV-1 and HIV-2 a tropism for CD4-bearing lymphocytes and monocyte macrophages and can also grow in vitro in human PBMCs. Although they infect some nonhuman primate species without causing disease, experimental infection of other susceptible nonhuman primate species has shown that SIVs can cause chronic wasting syndromes and a disease similar to AIDS (1). SIV is genetically and antigenically related to HIV-2, resulting in substantial serologic cross-reactivity (8). A recent report of SIV-like HIV-2 isolates among West African persons suggests the possibility that SIV and HIV-2 may represent a single group of viruses (9). In both laboratory workers reported here, the serologic reactivity detected cannot be differentiated from that of HIV-2.

The declining antibody titers following a peak 3-5 months after the exposure of the first patient suggest that the worker did not become persistently infected with SIV. However, persistence of antibody over 2 years and an increase in titer suggest that the second patient might have become infected. The implications of seroconversion without demonstrable infection and the health consequences of seroconversion for these workers are unknown.

This report reemphasizes the need for laboratory and animal workers in SIV research laboratories to strictly adhere to recommended guidelines and procedures while working with SIV (2). In both cases, departures from recommended safety procedures occurred: in the case of the percutaneous exposure, the vacutainer holder was disconnected before disposal of the contaminated needle; and in the second case, despite open skin lesions and without use of gloves, work was performed on clinical specimens. A similar case was reported of a laboratory worker with dermatitis on exposed skin who acquired HIV-1 infection in the laboratory (10).

The 3-month time lapse from exposure to seroconversion for the first worker emphasizes the need for a follow-up of at least 3-6 months for persons sustaining unintentional exposures to SIV. In addition, the whole-virus HIV-2 and SIV EIAs were less sensitive than peptide-based EIAs, HIV-2/SIV WBs, and RIPAs in detecting seroreactivity; therefore, investigation of persons sustaining exposures to SIV should include these sensitive assays.

The frequency of exposures in SIV research laboratories and the risk of seroconversion in SIV laboratory and animal-care workers have not been well defined. Approximately 200-300 persons are working with these agents in U.S. laboratories. CDC has investigated two other persons with percutaneous exposures involving cuts with scalpels during necropsies on SIV-infected animals. Neither have shown any evidence of seroconversion up to 6 months after the incidents. CDC, in collaboration with the National Institutes of Health, is conducting a serosurvey of workers in federally funded SIV research facilities to estimate the prevalence of such seroreactivity in persons with potential exposure to SIV.


  1. Letvin NL. Animal models for AIDS. Immunol Today 1990;11:322-6.

  2. CDC. Guidelines to prevent simian immunodeficiency virus infection in laboratory workers and animal handlers. MMWR 1988;37:693-4,699-704.

  3. Khabbaz RF, Rowe T, Murphey-Corb M, et al. Simian immunodeficiency virus needlestick accident in a laboratory worker. Lancet 1992;340:271-3.

  4. Villinger F, Powell JD, Jehuda-Cohen T, et al. Detection of occult simian immunodeficiency virus SIVsmm infection in asymptomatic seronegative nonhuman primates and evidence for variation in SIV gag sequence between in vivo- and in vitro-propagated virus. J Virol 1991;65:1855-62.

  5. Allan JS, Short M, Taylor ME, et al. Species-specific diversity among simian immunodeficiency viruses from African green monkeys. J Virol 1991;65:2816-28.

  6. Daniel MD, Letvin NL, King NW, et al. Isolation of T-cell tropic HTLV-III-like retrovirus from macaques. Science 1985;228:1201-4.

  7. Fultz PN, McClure HM, Anderson DC, Swenson RB, Anand R, Srinivasan A. Isolation of T-lymphotropic retrovirus from naturally infected sooty monkeys (Cercocebusatys). Proc Natl Acad Sci USA 1986;83:6286-90.

  8. Hirsch VM, Zack PM, Vogel AP, Johnson PR. Simian immunodeficiency virus infection of macaques: end-stage disease is characterized by widespread distribution of proviral DNA in tissues. J Infect Dis 1988;163:976-88.

  9. Gao F, Yue L, White AT, et al. Human infection by genetically diverse SIVsm-related HIV-2 in West Africa. Nature 1992;358:495-9.

  10. CDC. 1988 Agent summary statement for human immunodeficiency virus and report on laboratory-acquired infection with human immunodeficiency virus. MMWR 1988;37(S-4).

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