Recalcitrant pseudotumoral anogenital herpes simplex virus type 2 in HIV-infected patients: evidence for predominant B-lymphoplasmocytic infiltration and immunomodulators as effective therapeutic strategy.
BACKGROUND
In patients with human immunodeficiency virus (HIV) infection, genital herpetic lesions may be extensive and tend to persist for longer periods; in addition, atypical hypertrophic, ulcerative, or pseudotumor forms have been reported, frequently showing resistance to acyclovir (ACV) treatment.


METHODS
Between 2003 and 2011, 10 HIV-1-infected patients presenting with chronic pseudotumoral anogenital herpes simplex type 2 (HSV-2) infections were studied.


RESULTS
All patients developed chronic, hypertrophic HSV-2 anogenital lesions with multilesional presentation in 7 cases and involvement of 2 anatomical sites in 6 of them. At the time of diagnosis, the median CD3(+)CD4(+) absolute blood count was 480.5 cells/µL (range, 165-632 cells/µL), whereas the plasma HIV load was undetectable in all cases. Histopathologic analysis of lesion biopsies showed a moderately dense dermal polytypic plasma cell infiltrate. Detection of HSV-2 by culture and/or polymerase chain reaction was positive for all patients, with evidence for ACV-resistant strains in 6 of 8 cases. In addition, viral resistance to ACV was found only in HSV-2 isolated from ulcerative lesions, whereas purely pseudotumoral ones harbored sensitive strains. Durable control was observed with HSV DNA polymerase inhibitors in only 2 cases, and the immunomodulators imiquimod and thalidomide allowed 5 patients to reach sustained complete response.


CONCLUSIONS
HSV-2-related pseudolymphoma in HIV-infected patients is characterized by a predominant polyclonal lymphoplasmacytic infiltration, and is frequently refractory to antiherpetic drugs. Immunomodulatory therapeutic strategies using thalidomide showed consistent efficacy, and should be considered early during the course of disease.
UPEC, LIC EA 4393 and Department of Dermatology, AP-HP Hôpital Henri Mondor, Créteil.
Emilie
E
Sbidian
Maxime
M
Battistella
Jérome
J
Legoff
Matthieu
M
Lafaurie
Maud
M
Bézier
Félix
F
Agbalika
François
F
Simon
Fabrice
F
Bouscarat
Jean-Michel
JM
Cayuela
Guislaine
G
Carcelain
Nadira
N
Houhou
Martine
M
Bagot
Jean Michel
JM
Molina
Michel
M
Janier
Hervé
H
Bachelez
D000212:Acyclovir / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use; D024882:Drug Resistance, Viral; D005260:Female; D015658:HIV Infections / Q000821:virology*; D006558:Herpes Genitalis / Q000473:pathology / Q000628:therapy* / Q000821:virology*; D018258:Herpesvirus 2, Human / Q000187:drug effects / Q000302:isolation & purification*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D013792:Thalidomide / Q000627:therapeutic use; D013937:Thymidine Kinase / Q000235:genetics
D000998:Antiviral Agents; D007166:Immunosuppressive Agents; D013792:Thalidomide; D013937:Thymidine Kinase; D000212:Acyclovir
AIDS; HIV; acyclovir-resistant HSV infection; human immunodeficiency virus; pseudotumoral anogenital herpes