A. Del Mistro

HPV-related neoplasias in HIV-infected individuals

Human papillomavirus (HPV) infection of the lower genital tract is now considered the most important factor in the initiation of neoplasia. Human immunodeficiency virus (HIV) infection appears to alter the natural history of HPV-associated oncogenesis, but its impact on gynaecology has only recently been defined; the Centers for Disease Control (CDC) designated moderate and severe cervical dysplasia as a category B defining condition, and invasive cervical cancer as a category C defining condition of AIDS in 1993. Anal HPV infection and anal squamous intra-epithelial lesions have been found to be highly prevalent among HIV-positive homosexual men, and recent preliminary data suggest a relatively high prevalence among HIV-positive women as well. Moreover, HPV infection and associated lesions are also observed in body sites other than the anogenital area, particularly the skin and the oral cavity.

HTLV-I and HTLV-II infections among HIV-1 seropositive patients in Sao Paulo, Brazil.

To estimate the presence of, and the risk factors for HTLV-I and HTLV-II infections among HIV-1 infected subjects in Sao Paulo, Brazil, a serosurvey was performed in 471 HIV-1 infected patients, including 216 intravenous drug addicts (IVDA), 229 homosexual/bisexual men, and 26 with other risk factors. Serum samples were screened for HTLV seroreactivity by ELISA; reactive samples were analyzed by Western Blot (WB), using whole HTLV-I lysate as antigen. To confirm and discriminate HTLV-I and HTLV-II infections, sera presenting any bands on WB were further analyzed by a WB containing recombinant HTLV-I and HTLV-II proteins (WB 2.3), and by enzyme immunoassays using synthetic peptides specific for envelope proteins (Synth-EIA). In 22 cases, cell samples were available for polymerase chain reaction (PCR) studies. On WB, 114 sera were reactive and, of these, 37 and 25 were concordantly positive on both WB 2.3 and Synth-EIA procedures for HTLV-I and HTLV-II specific antibodies, respectively; 37 specimens were negative on both assays, and 15 gave discordant or indeterminate results. PCR findings confirmed concordant results obtained in the discriminatory serological assays. The prevalence rates of HTLV-I and HTLV-II infections were 15.3% and 11.1% in IVDA, and 0.9% and 0.4% in homosexual/bisexual men, respectively. No case of HTLV-I/HTLV-II co-infection was found.

Immunological markers in the cerebrospinal fluid of HIV-1-infected children.

ABSTRACT. Several immunological abnormalities were detected in the cerebrospinal fluid (CSF) of human immunodeficiency virus type 1 (HIV‐1)‐infected children. Intrathecal synthesis of immunoglobulins, free light chains (FLC), IL‐1β, IL‐6, and M‐CSF were demonstrated both in asymptomatic children and children with subacute encephalopathy. Our findings further support the hypothesis that an immunopathological subclinical process within the central nervous system (CNS) may be an early manifestation of acquired immunodeficiency syndrome (AIDS). Cytokine detection in the CSF may represent a useful diagnostic tool in evaluating the outcome of HIV‐1‐infected patients.

First case in Italy of fatal AIDS in a hemophiliac

The first fatal case of AIDS in an hemophiliac observed in Italy is reported. The propositus is a 53-year-old hemophilia A patient who died on the 8th December, 1984. AIDS was documented clinically and in the laboratory by serum antibodies to HTLV-III detected by ELISA and Western blot assays. A progressive intellectual worsening of the patient due to diffuse cerebral atrophy was followed by CT scan, EEG and by evaluation of proper neurological signs and symptoms.

HOW FREQUENT AND HOW EARLY DOES THE NEUROLOGICAL INVOLVEMENT IN HIV-POSITIVE CHILDREN OCCUR ? PRELIMINARY RESULTS OF A PROSPECTIVE STUDY

To study the natural history of the neurological involvement in pediatric human immunodeficiency virus (HIV) infection, 77 children born to seropositive mothers have been followed up since birth. The median follow-up time has been 17.5 months. Fourteen children were classified as infected, 34 as not infected, and 21 as indeterminable. Only two children with full-blown acute immune deficiency syndrome had severe neurological manifestations. “Soft” neurological signs were found in six infected, and ten non-infected children (χ2, P<0.05). The mean development quotient and IQ scores in the infected and the non-infected children were 82.22, and 93.15, respectively (Mann-Whitney test, P>0.05). These data suggest that neurological and developmental abnormalities do not occur early in the course of vertical HIV infection and that they are associated with severe immunodeficiency.

B Cell Activation and HIV-1 Infection

The human immunodeficiency virus type 1 (HIV-1), the causative agent of the acquired immunodeficiency syndrome (AIDS) in man, shows tropism for CD4+ T cells mostly, and this accounts for the intense impairment in cellular immunity function (for review, see Rosenberg and Fauci 1989); however, B cell function is also severely deranged by HIV-1 infection (for review, see Amadori and Chieco-Bianchi 1990). Although the biologic properties of HIV-1, and its life cycle in the host are well understood, a comprehensive view of the pathogenesis of AIDS is still lacking, and it is still debated whether the T cell deficiency depends only on the virus’ cytopathic effect, or whether other mechanisms also come into play. Among the pathways proposed as co-factors in generating AIDS, the possibility that B cell deregulation might be involved is intriguing. This article reviews current knowledge on the features characterizing B cell function during HIV-1 infection, and addresses the possible participation of the humoral compartment in the pathogenesis of AIDS and associated disorders.

Prevalence of HIV infection in a cohort of patients with congenital coagulation defects of the prothrombin complex factors.

Twenty-seven patients suffering from congenital coagulation defects of the prothrombin complex factors were investigated: six had haemophilia B; 14, factor VII defect; four, factor X defect; and three, factor II defect. Nineteen patients (70.3%) had previously received plasma and/or clotting factors concentrates. Among these, markers of hepatitis B infection (HBV) were present in five cases (26.3%) and hepatitis C (HCV) antibodies were found in seven cases (36.8%). The HIV1 prevalence was similarly high. In fact, five patients (26.3%), previously infused with factor IX or prothrombin complex factors concentrates, developed HIV1 infection. No patient with factor VII deficiency became HIV1 positive, despite the administration of unheated factor VII concentrates and the consequent HBV and HCV contamination. In the HIV1 positive group, three patients showed a false positivity for HIV2 antibodies. Five years after seroconversion, three patients developed AIDS (stage IV) and died, one had persistent generalized lymphadenopathy (stage III), and one with post-hepatitis liver cirrhosis was asymptomatic (stage II) for HIV infection. The significant decrease in total white cells, T4 lymphocytes and platelet counts and increase of beta 2-microglobulin and neopterin levels confirmed the prognostic value of these markers for the progression of HIV1 disease. Only one HIV1 negative transfused patient developed anti-HTLV-I p19 antibodies.

Immunological Findings in the CSF of HIV-1 Infected Patients

Both peripheral and central nervous system disorders have been described in patients with the acquired immunodeficiency syndrome (AIDS).1–8 Increasing evidence indicates that the human immunodeficiency virus type 1 (HIV-1) is neurotropic and infects the nervous system early in the course of systemic virus spread.9–14 Ultrastructural and hybridization analyses of brain tissue from AIDS patients have revealed that HIV-1 replication occurs predominantly in cells of macrophage/microglial lineage.15–16 However, the relationship between the neurological/psychiatric symptoms associated with HIV-1 infections of the central nervous system (CNS) and the HIV-1-induced immunological abnormalities at the cellular level is still unclear.

No evidence of HIV-2 infection in subjects at risk for aids living in North-East Italy

Sera samples from 1134 individuals (824 HIV-1 seropositive and 310 HIV-1 seronegative), collected from January 1988 to April 1990, were tested for HIV-2 antibodies by whole virus assays and synthetic peptide-based assays to determine the prevalence of HIV-2 infection in populations at risk for AIDS in North-East Italy (Veneto Region). Partial reactivities on HIV-2 Western Blot were a common finding in HIV-1 seropositive samples. None of the sera fulfilled the criteria for HIV-2 seropositivity, since only low-level reactivity was observed with an HIV-2 competitive ELISA test, and no reactivity occurred with an HIV-2 specific peptide.Therefore, there is no evidence of HIV-2 infection in this geographical area, to date.