S201 The human papillomavirus family

S46

Symposia

-

Genital

Human

Papillomaviruses

mor, although irmnunosuppression is not a prerequisite for its development. On the other hand, in 10 pts with HIV-associated KS, high viral loads were measured recently by HIV-l RNA assay (>lflOOOO cop/ml), thus suggesting that high levels of HIV viremia may promote clinical manifestation of KS. In one particular patient showing most rapid KS development and progression after seroconversion together with CD4+ cell depletion a novel, syncytium-inducing HIV- 1 B subtype variant has been detected. Statistical analysis of the entire group performed on 190 matched pairs with and without HIV-associated KS revealed that presence of KS is a risk factor for survival per se, independent from the CD4+ cell counts. Overall, the development and progression of KS may be related to (a) an additional tumorigenic agent, (b) the severity of HIV-infection (viral load), (c) the extent of immunosuppresion and, (d) the HIV-subtype, all being responsible for its growth. Early antiretroviral treatment seems required in HIV-associated KS, possibly reducing the risk for its development and/or influencing its clinical course.

- The Way Forward

host. The clinical and evolutive parameter remains, still today, the guidance criteria of the systemic and local therapies which are by now known. For rapidly evolutive classical KS, angiomatous or complicated: monochemotherapy in lst, 2nd or 3rd instance (VLB, VNR, VP16 os/ev, BLM); polichemotherapy in 4th instance (ABV). For iatrogenic KS: reduction of the immunosuppressive therapy, possibly associated to monochemotherapy. For visceral correlated KS-AIDS, at rapid progression, with aesthetic-functional compromission: therapy with interferon-alpha or with a mono- or polichemotherapy (VCR, VLB, VP16, DXR, BLM, VCR + VLB, VCR + BLM, DXR + BLM) associated to antiretroviral therapy. New therapeutic strategies, even though not sustained by wide cases, derive from the use of paclitaxel and of inhibitors of cytokines (such as TNF, growth factor, TAT gene product). If the discovery of the infectious etiologic factor of KS by Chang and co11 will be confirmed and the antihetpesviral therapies (gancyclovir, foscamet) will reveal themselves as efficient in reducing the risk of KS, new trials will be possible for future completely new therapies.

I Si 98 New insights in the differences between

classical and HIV-associated Kaposi’s sarcoma

D. Cerimele’ , F. Cottoni *. ‘Dept. University, Italy

Rome;

*Dept.

Dermatology, Dermatology, University

Catholic of Sassari,

Kaposi’s sarcoma (KS) very probably is a single disease. Anyway differences may be observed at clinical, histological, evolutionary and therapeutical levels between classic and HIV associated KS. Classic KS develops preferentially in the feet and lower legs of old men, while HIV associated KS develops preferentially on the trunk and neck with pityriasis rosea-like lesions, on the face, oral and gastric mucosa, lymph nodes, internal organs (lungs, liver). Vascular formations of slit-like blood vessels, intermingled with spindle cells bundles, with few extravasated erithrocytes and deposits of hemosiderin are observed; in HIV-associated KS early lesions with irregular vascular spaces; incompletely lined with endothelial cells, sometimes surrounding normal pre-existing blood vessels, with more abundant extravasated erythrocytes, are observed. The evolution of classical KS is indolent or slowly progressive, with few exceptions. HIV-associated KS on the contrary is rapidly progressive. The response to treatment is also different: classic KS may be treated with less aggressive schedules (radiotherapy, vinca alkaloids, low-dose interferon), while HIV-associated KS needs more aggressive treatment (high-dose interferon, polichemotherapy). ElS199 The therapy of Kaposi’s sarcoma: Current

status and future directions

L. Brambilla. Institute Maggiore,

Milan,

of Dermatology,

IRCCS

Ospedale

Italy

The clinical experience, which today is supported by the identification of the a new herpes virus associated to Kaposi’s sarcoma (KSHV), proposes the KS as a one and only entity, whose etrogeneous behaviour is most likely conditioned by the

IS200

Now: What’s really new?

Constantin Orfanos. Germany Abstract not available.

Genital Human Papillomaviruses The Way Forward S201 El

The human papiiiomavirus

family

Marc Van Ranst. Belgium Abstract not available.

1S202 ( Epidemiology of genital papiiiomavirus infection Jorma Paavonen. Department University

of Helsinki,

of Obstetrics

and Gynecology,

Finland

Sexually transmitted human papillomavirus (HPV) infections cause major medical, social, and economic problems. HPV is the most common cause of viral sexually transmitted infections (STD. The spectrum of genital HPV infection ranges from genital warts to invasive anogenital cancer. HPV infections are strikingly prevalent. However, epidemiologic data of genital HPV infections are extremely variable for several reasons (e.g. differences in study populations, sampling techniques, or HPV detection assays). Significant differences in HPV prevalence have been found between younger and older women suggesting that genital HPV infections are age-dependent, decreasing with increasing age. This suggests that most HPV infections are transient. However, HPV positivity among women who develop anogenital neoplasia remains high regardless of age which suggests that some women develop persistent infections. Persistence is higher among those infected by high risk HPV