Morbidity and Mortality Weekly Report Vol. 41, no. 36

680

MMWR

September 11, 1992

Seroconversion to SIV - Continued
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: 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-Iike 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.