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Infection and Immunity, April 1999, p. 1569-1578, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Phase Variations of the Mycoplasma penetrans Main Surface Lipoprotein Increase Antigenic Diversity

Olivier Neyrolles,1,dagger Isabelle Chambaud,1 Stéphane Ferris,1 Marie-Christine Prevost,1 Tsuguo Sasaki,2 Luc Montagnier,1 and Alain Blanchard1,*

Unité d'Oncologie Virale, Institut Pasteur, 75724 Paris Cedex 15, France,1 and Department of Safety Research on Biologics, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo 208-0011, Japan2

Received 23 June 1998/Returned for modification 28 September 1998/Accepted 5 January 1999

Mycoplasma penetrans is a recently identified mycoplasma, isolated from urine samples collected from human immunodeficiency virus (HIV)-infected patients. Its presence is significantly associated with HIV infection. The major antigen recognized during natural and experimental infections is an abundant P35 lipoprotein which, upon extraction, segregates in the Triton X-114 detergent phase and is the basis of M. penetrans-specific serological assays. We report here that the P35 antigen undergoes spontaneous and reversible phase variation at high frequency, leading to heterogeneous populations of mycoplasmas, even when derived from a clonal lineage. This variation was found to be determined at the transcription level, and although this property is not unique among the members of the class Mollicutes, the mechanism by which it occurs in M. penetrans differs from those previously described for other Mycoplasma species. Indeed, the P35 phase variation was due neither to a p35 gene rearrangement nor to point mutations within the gene itself or its promoter. The P35 phase variation in the different variants obtained was concomitant with modifications in the pattern of other expressed lipoproteins, probably due to regulated expression of selected members of a gene family which was found to potentially encode similar lipoproteins. M. penetrans variants could be selected on the basis of their lack of colony immunoreactivity with a polyclonal antiserum against a Triton X-114 extract, strongly suggesting that the mechanisms involved in altering surface antigen expression might allow evasion of the humoral immune response of the infected host.

* Corresponding author. Mailing address: Unité d'Oncologie Virale, Institut Pasteur, 28, rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: (33-1)-40-61-31-31. Fax: (33-1)-40-61-34-65. E-mail: ablancha{at}pasteur.fr.

dagger Present address: Imperial College School of Medicine at St. Mary's, Department of Medical Microbiology, London, W2 1PG, United Kingdom.

Infection and Immunity, April 1999, p. 1569-1578, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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