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Biomedical subjects

M Corbellino

Publications and source records attributed to M Corbellino.

36 records · Page 2Linked to original sources
PubMed1997

Homozygous delta 32 deletion of the CCR-5 chemokine receptor gene in an HIV-1-infected patient.

BACKGROUND: Recent research has found that entry of non-syncytium-inducing (NSI), monocyte-macrophage-tropic HIV-1 isolates requires binding to both CD4 and CCR5 receptors, and that delta 32/delta 32 homozygous individuals are protected against infection. OBJECTIVE: To analyse the polymorphism of CCR-5 gene in HIV-1-infected and uninfected subjects. DESIGN AND METHODS: CCR-5 sequences were amplified by polymerase chain reaction (PCR) from DNA of peripheral blood mononuclear cells. Samples from 152 HIV-1-infected subjects and 122 uninfected controls were tested for the detection of the 32 base-pair deletion. HIV-1 phenotype was determined by viral isolation and MT-2 evaluation. RESULTS: The wild-type/delta 32 heterozygous and delta 32/delta 32 homozygous conditions were represented in 10.7 and 0.8% of healthy controls and in 9.8 and 0.7% of HIV-1-infected subjects, respectively. Of note, the delta 32/delta 32 deletion of the CCR-5 gene was detected by PCR and sequencing confirmed in a patient with progressive infection harbouring a clade B virus with SI phenotype. CONCLUSIONS: delta 32/delta 32 homozygosity for the CCR-5 gene does not confer absolute protection against HIV-1 infection, suggesting that either macrophage-tropic viral strains could use coreceptors other than CCR-5 or infect independently of the presence of a functional CCR-5 coreceptor. Alternatively, primary infection sustained by T-cell-tropic isolates, although exceptional, may occur.

Adult↗
PubMed1997

Simultaneous onset of primary cutaneous B-cell lymphoma and human herpesvirus 8-associated Kaposi's sarcoma.

We report the simultaneous occurrence of Kaposi's sarcoma (KS) and primary cutaneous B-cell lymphoma (CBCL) of the leg in a 79-year-old woman, seronegative for HIV-1, HTLV-1 and HTLV-2. The CBCL underwent complete clinical remission after local radiotherapy, whilst the KS became disseminated within a year following diagnosis. However, 2 years after the diagnosis of KS, the patient died with neurological symptoms. These were presumed to be due to involvement of the central nervous system by lymphoma, although in the absence of an autopsy, this could not be proven. Skin biopsies from the original KS and CBCL lesions, as well as short-term culture of spindle cells from the KS lesion and peripheral blood mononuclear cells (PBMC), were studied by semiquantitative polymerase chain reaction (PCR) using primers specific for DNA sequences of a novel gamma-herpesvirus-8 (HHV-8). PCR studies were strongly positive for the virus on KS cells and PBMC; conversely, a low viral load was found on CBCL cells. A high titre of serum IgG antibodies reacting with the nuclei of the HHV-8 positive cell line BCP-1 was found. These data suggest that reactivation of latent infection with HHV-8 had occurred in this patient, and that HHV-8 is directly involved in KS, but not in CBCL of the leg, an aggressive variant of CBCL.

Aged↗
PubMed1997

Expression of a virus-derived cytokine, KSHV vIL-6, in HIV-seronegative Castleman's disease.

Castleman's disease is a rare B cell lymphoproliferative disorder related to excess interleukin-6 (IL-6)-like activity. Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8), which encodes a functional cytokine (vIL-6), has been found in some patients with Castleman's disease. Lymph nodes from 14 HIV-seronegative Castleman's disease patients were compared to hyperplastic lymph nodes from 25 HIV-seronegative patients as well as Kaposi's sarcoma lesions from 48 patients for KSHV infection and vIL-6, human IL-6, and Epstein-Barr virus EBER expression. While all Kaposi's sarcoma tissues examined were polymerase chain reaction-positive and all control lymph nodes were polymerase chain reaction-negative for KSHV, none had detectable vIL-6 expression. Six of 14 (43%) Castleman's tissues were positive for KSHV by polymerase chain reaction and all 6 had evidence of vIL-6 expression by immunohistochemistry. vIL-6-positive Castleman's disease patients generally had the multicentric plasma cell variant form of the disease and had a rapidly fatal clinical course frequently associated with autoimmune hemolytic anemia and gammopathy. In contrast, 7 (88%) of the 8 vIL-6-negative Castleman's disease patients had localized disease and have remained disease-free after therapy. KSHV vIL-6 expression appears to be limited to hematopoietic cells and is not present in Kaposi's sarcoma spindle cells. These data suggest that Castleman's disease is a syndrome of multiple etiologies involving aberrant IL-6 activity from either endogenous or viral sources.

Adolescent↗
PubMed1996

Restricted tissue distribution of extralesional Kaposi's sarcoma-associated herpesvirus-like DNA sequences in AIDS patients with Kaposi's sarcoma.

Specific herpesvirus-like DNA sequences have been found in Kaposi's sarcoma (KS) lesions of AIDS patients, suggesting that a novel gamma herpesvirus, homologous to Epstein-Barr virus and herpesvirus saimiri, could be implicated in the pathogenesis of KS. To better understand the role of this putative etiological agent, named Kaposi's sarcoma-associated herpesvirus (KSHV) or human herpesvirus 8 (HHV-8), we investigated by the polymerase chain reaction (PCR) the presence of viral DNA sequences in various organs obtained at autopsy from seven AIDS patients with KS and six without KS. For each sample, to exclude positive results due to visceral KS dissemination, the presence of microscopic foci of KS cells was rules out by histology and CD34 immunohistochemistry on serial frozen sections immediately adjacent to those employed for DNA extraction. PCR and nested PCR were performed with primers specific for the HIV-8 330 Bam fragment originally described by Chang et al. (Science 1994;266:1865-1869). As quality control, the extracted DNA was amplified with primers for human beta-globin. All KS legions were HHV-8 positive. In addition, extralesional KSHV DNA sequences were detected in seven of seven lymphoid organs and in five of five prostate glands of KS patients. Normal skin was positive in three of five cases and bone marrow in two of three tested cases, all other tissues being negative by PCR and nested PCR. By contrast, no virus was detected in tissue samples of AIDS cases without KS. The restricted organ distribution here documented argues for a selective tissue tropism of HHV-8 in vivo in AIDS patients and suggests that in the infected host lymphoid organs and the prostate gland may represent privileged sites of viral latency and persistence.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Human herpesvirus 6 infects cervical epithelial cells and transactivates human papillomavirus gene expression.

To examine whether human herpesvirus 6 (HHV-6) is capable of infecting human cervical epithelial cells and altering expression of human papillomavirus (HPV) genes, HPV-immortalized or -transformed carcinoma cell lines were infected with HHV-6 variant A. No cytopathic effect was observed in infected cervical cells. However, immunofluorescence indicated that infected cells expressed early-late proteins of HHV-6 by day 3 postinfection. HHV-6 DNA was also detected by Southern blot hybridization after infection and persisted through continued subculture in an episomal state as proven by Gardella gel electrophoresis and fluorescence in situ hybridization. HHV-6 infection enhanced expression of HPV RNAs encoding the viral oncoproteins E6 and E7. Transient transfection assays showed that two HHV-6 molecular clones, pZVB-70 and pZVH-14, upregulated transcription 9- to 15-fold from a receptor plasmid containing the HPV type 18 regulatory sequences which control transcription in vivo. Cervical carcinoma cells infected with HHV-6 induced more rapid development of tumors in mice than did noninfected cells. These results are the first evidence that human cervical epithelial cells can be infected with HHV-6 and that HHV-6 contains transactivators which stimulate the HPV-transforming genes.

Animals↗
PubMed1989

Clinical and immunological aspects of HIV infection in drug addicts.

Intravenous drug users (IVDUs) account for more than 64% of the total AIDS cases in Italy. The IVDUs' seropositivity rate is greater than 70% in Milan and greater than 50% in the main cities of Italy. The first evidence of seropositivity in this population dates back to 1979. In a cohort study performed in Milan the rate of progression to overt AIDS among IVDUs was 6% in 3 years (1984-1987). At presentation, more than 75% of the subjects had CD4+ cell counts higher than 400/mm3 (mean 631, median 528, mode 465). These values are significantly higher than those observed in the same population in New York, the only American city with HIV-infection spread comparable to that observed in Milan. The probability of having CD4+ cell counts lower than 400, 300, and 200/mm3 in relation to the length of follow-up was, respectively, 50, 40, and 2% after 36 months from presentation. At the same end point, subjects presenting less than 400 CD4+ cells at entry had 30% probability of falling under 200 cell/mm3. The pattern of CD4+ cells, as much as the low percentage of yearly progression to overt AIDS, is probably related to the recent, even if rapid, spread of infection among IVDUs in Italy. The clinical features of overt AIDS present some differences between IVDUs and other at-risk groups. Among U.S. IVDUs with AIDS, Kaposi's sarcoma is infrequent (2.9% vs 27.7% in homosexual men) while mycotic infections such as deep candidiasis and cryptococcosis are significantly more frequent. The same pattern has been observed in our case file in Milan: esophageal candidiasis represents the most frequent cause of diagnosis of overt AIDS. Mycotic infections, overall, are more frequent than in U.S. IVDUs. The increased rate of mycotic infections among IVDUs might be justified by altered functions of nonspecific immunity, such as PMNL killing and phagocytosis of Candida albicans spores, impaired in HIV-infected IVDUs, but generally normal in infected subjects belonging to the other at-risk groups.

CD4-Positive T-Lymphocytes↗
PubMedDate not supplied

[Disseminated histoplasmosis in patients with AIDS. 2 case reports].

Histoplasmosis is endemic in some areas of United States and in South America, and generally causes an acute self-limiting respiratory infection. In elderly and immunosuppressed patients the infection can spread through the blood, causing a severe systemic illness. Here we describe two cases of disseminated histoplasmosis in AIDS patients. The first was observed in an Italian woman who had never visited endemic countries, and was recognized only at autopsy; the second was observed in a trans-sexual patient, arrived in Italy from Brazil. Clinical suspicion of histoplasmosis is important in immunocompromised patients of non-endemic areas as symptoms are often aspecific and misdiagnosis is frequent.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Lymphangiosarcoma of the pubic region: a rare complication arising in congenital non-hereditary lymphedema.

Lymphangiosarcoma is a rare, aggressive, vascular neoplasm arising in chronic congenital or acquired lymphedema. Although it is most frequently associated with post-mastectomy lymphedema (Stewart-Treves's syndrome), lymphangiosarcoma can exceptionally arise in congenital hereditary lymphedema (Milroy's syndrome and Meige's syndrome) and non-hereditary lymphedema (congenital, praecox or forme tarde lymphedemas). We report a case of lymphangiosarcoma of the pubic region, supported by immunohistochemical studies, in a 42-year-old woman affected by congenital, non-hereditary lymphedema of the left genital region and homolateral lower limb. In addition, molecular analysis demonstrated the absence of Kaposi's sarcoma-associated Herpes virus (KSHV) DNA sequences in tumour lesions. To our knowledge, this is the first case of lymphangiosarcoma associated with congenital non-hereditary lymphedema confined to the pubic region. The literature concerning the cases of lymphangiosarcoma arising in congenital hereditary and non-hereditary lymphedema is reviewed. Moreover, we emphasized the importance of regular clinical controls in all patients affected by chronic lymphedema. In fact, although the prognosis of this neoplasm is very poor, a prompt diagnosis and a rapid, ablative surgery associated with radiation therapy can increase the possibility of survival of these patients.

Adult↗