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

Vol. 41 1 No. 36

MM WR

679

Seroconversion to SIV - Continued
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) gp4l 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 gpl30 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 (pot) (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, pot, 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 SI V-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).