HIV type 1 env subtype E in Cambodia.

91 SINCE THE FIRST human immunodeficiency virus type 1 (HIV1) infection was detected in a blood donor in the Cambodian capital of Phnom Penh in 1991, HIV-1 has spread rapidly in this Southeast Asian country.1 Rates among blood donors rose from 0.08% in 1991 to 4.5% in 1995.1 In that latter year, median HIV rates in sentinel seroprevalence surveys were 37.9% in commercial sex workers (CSWs), 8.1% in soldiers, and 2.6% in pregnant women, who likely reflect HIV trends in the general population. All of the available HIV/AIDS surveillance data indicate that the HIV epidemic in Cambodia is almost exclusively among heterosexuals, along with some perinatal infection.1,3 To date, there is little evidence for spread by injecting drug use. In contrast to the extensive knowledge of the genetic subtypes of HIV-1 causing the epidemic in neighboring countries, little is known concerning those in Cambodia. Env subtype E was identified in seven Indonesian,5,6 five French,7 and five Uruguayan8 soldiers who returned from the peace-keeping mission for 21-nation United Nation Transition Authority Cambodia (UNTAC) (one Uruguayan soldier was infected with subtype B). But temporary transit and recreational travel by such troops in adjacent Thailand create uncertainty about the actual source of such infections. We used genetic and serologic techniques to confirm the subtype of HIV-1 circulating in Cambodian nationals. In March and April 1996, whole blood specimens were collected in Phnom Penh from nine consenting Cambodians previously identified as HIV seropositive. Six were men infected through sexual contact, one (C202) was the wife of one of these men (C201), and two were blood donors whose routes of infection were unknown (Table 1). Although the patients originated in different parts of the country, neither the location where infection was acquired, nor the duration of infection, was known. Genetic analysis were performed as described previously.9 Briefly, peripheral blood mononuclear cells (PBMCs) were separated by Ficoll-Hypaque (Pharmacia LKB, Uppsala, Sweden) centrifugation. DNAs were extracted from PBMCs by QIAamp blood kit (Qiagen, Chatsworth, CA). The C2/V3 regions of HIV-1 proviral env genes were amplified by nested polymerase chain reaction (PCR) with outer primer pairs TAT-001A (identical to MK369) (59 -TGGAGCCAGTAGATCCTAGAC TAGAGCCCT-3 9 ) and TM-020B (identical to MK616) (59 -