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Antibodies have been raised against a synthetic peptide (IRDKIQKENALFRNL) containing a neutralizing epitope within the second variable region of the human immunodeficiency virus type 1 (HIV-1) SF2 strain external envelope glycoprotein (gpl20) and also against equivalent peptides of the HIV-1 LAI, RF and MN isolates. The resulting antisera cross-react with heterologous peptides but binding to heterologous recombinant gpl20 is more restricted. Antisera to HIV-1 SF2, RF and MN are able to neutralize homologous virus.Some cross-neutralization is also observed, but a consensus peptide failed to induce neutralizing antibodies to any of the isolates studied. Antibodies to the V2 and V3 epitopes give a higher neutralization index when acting together than when the individual sera are used alone. Antibodies induced in natural infection bind to two sets of hexamers within the region encompassed by the 15-mer peptide, and the response to these can differ between infected individuals and within the same host over time.

A questionnaire was circulated to all lead genitourinary (GU) medicine physicians in the UK in November 2003 to obtain data on access, waiting times and triaging. Of the 143 responders, 92.3% departments had limited access to some or all GU medicine clinics. Where access was limited, 5.3% had no identifiable process in place to see urgent patients. The mean waiting times in clinics with an open appointment system only for a routine female and male appointment were 2.9 weeks and 2.8 weeks (range 2 days-10 weeks), respectively, and for an urgent appointment, two days (range same day-14 days), for both sexes. The survey has raised concerns that a number of departments did not consider as urgent for prioritizing, patients with documented untreated gonorrhoea, syphilis, or HIV, or contacts of patients with these conditions. This survey has highlighted a need for the national specialist society to provide guidance on prioritizing patients where access is limited.

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Further research addressing the following questions is needed to elucidate the clinical significance of this finding: Is MG a sexually transmitted pathogen among MSM warranting more clinical attention? Should MG be included in routine screening of MSM? What is MG's role in infectious proctitis and the transmission of other pathogens such as HIV? REFERENCES 1 Jensen JS. Mycoplasma genitalium: the aetiological agent of urethritis and other sexually transmitted diseases. J Eur Acad Dermatol Venereol 2004;18:1-11 2 Bradshaw CS, Fairley CK, Lister NA, Chen S, Garland SM, Tabrizi SN. Mycoplasma genitalium in men who have sex with men at male-only saunas. Sex Transm Infect 2009;85:432-5 3 Taylor-Robinson D, Gilroy CB, Keane FE. Detection of several Mycoplasma species at various anatomical sites of homosexual men. Eur J Clin Microbiol Infect Dis 2003;22:291 -3 4 Francis SC, Kent CK, Klausner JD, et al. Prevalence of rectal Trichomonas vaginalis and Mycoplasma genitalium in male patients at the San Francisco STD clinic, 2005 -2006. Sex Transm Dis 2008;35:797 -800 5 Taylor-Robinson D, Furr PM, Hanna NF. Microbiological and serological study of non-gonococcal urethritis with special reference to Mycoplasma genitalium. Genitourin Med 1985;61:319-24 6 Jensen JS, Orsum R, Dohn B, Uldum S, Worm AM, Lind K. Mycoplasma genitalium: a cause of male urethritis? Genitourin Med 1993;69:265 -9 7 Baseman JB, Dallo SF, Tully JG, Rose DL. Isolation and characterization of Mycoplasma genitalium strains from the human respiratory tract.