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Biomedical subjects

F Lillo

Publications and source records attributed to F Lillo.

44 records · Page 3Linked to original sources
PubMedDate not supplied

HIV-1 DNA and RNA kinetics in primary HIV infection.

BACKGROUND: HIV-1 reservoir is early established during PHI. It is reduced, but not extinguished by early therapy: DNA containing cells are still detectable after months of successful viremia suppression. To define the best method to measure low level viral replication, we determined the extent of HIV reservoir in 11 acutely infected patients and evaluated how it is renewed even during successful treatment. METHODS: Eleven acutely infected HIV patients were included in the study. Three where not treated with antiretroviral drugs while 8 underwent early aggressive antiretroviral treatment (HAART) which, in 3 cases, was associated to cyclosporin A (CsA) administration. HIV viremia was monitored by commercially available methods while HIV-DNA and cellular RNA quantitation were obtained by in house PCR and RT-PCR respectively, in the gag region. RESULTS: Significant CD4 recover and HIV viremia suppression were reached in a mean period of three to six months in all treated patients. The course of the HIV-DNA and of cellular HIV RNA reduction showed a similar trend. This variation was slower, if compared to plasma viremia and never reached undetectable levels, justifying the rebound of viremia observed at therapy interruption. CONCLUSIONS: These data suggest and confirm that complete abolition of viral replication is not achieved and viral reservoir may be re-expanded even after short term rebound of viremia. Scheduling of possible structured therapy interruption should be designed based on multiple virological parameters and on the individual characteristics of the patients.

Adult↗
PubMedDate not supplied

Granulocyte/monocyte apheresis induces sustained increases in CD4 T cells in HIV-1 infected patients with poor CD4 T cell restoration after suppression of viral replication by HAART.

Current antiretroviral regimens (HAART) are generally effective in reducing viral replication to undetectable levels and inducing a raise in CD4 T cells. However, in approximately 5 to 15% of patients suppression of viral replication is not followed by an increase in CD4 T cells. Such patients may be at increased risk for opportunistic infections. Here we report the results from a phase II open label randomised trial on 30 patients classified as poor responders to HAART who were either subjected to eight consecutive cycles of selective monocyte apheresis or maintained under HAART alone. The results show that monocyte apheresis results in increased CD4 T cell counts which are maintained for at least 31 weeks after last apheresis. This effect was observed only on patients with complete suppression of viral replication. Other effects of monocyte apheresis included a strong reduction of TNF-alpha production in patients with high baseline levels of this cytokine and activation of resting T cells during the apheresis cycles. In two patients with high cellular HIV DNA load apheresis was followed by a 98% reduction, suggesting purging of infected cells. There was no evidence of increased viral replication during or after the apheresis cycles. The data show that monocyte apheresis is safe, well tolerated and may be indicated in patients who respond poorly to HAART.

Adult↗
PubMedDate not supplied

The effect of HAART on humoral immune response in primary HIV-1 infected patients.

The effect of Highly Active Antiretroviral Therapy (HAART) on binding and neutralizing antibody responses to human immunodeficiency virus type-1 (HIV-1) during primary and chronic infection was investigated. Seven patients HAART treated during primary infection, six HAART treated during chronic infection and five patients treated only with ZVD (Zidovudine) were analysed. HAART inhibited the development of anti env antibodies during primary infection. Administering HAART during primary infection usually did not substantially affect the development of weak neutralizing antibody responses against autologous virus. However, we demonstrated that very early treatment, during seroconversion, induce in some cases, a strong neutralizing antibodies against autologous virus. These results may be relevant for understanding how HAART may elicit a strong protective responses and may be useful in developing new strategies designed to achieve a long term control of the HIV infection.

Acute Disease↗
PubMedDate not supplied

Heterogeneity in exposed uninfected individuals.

In spite of repeated exposures to HIV, some individuals remain seronegative and apparently uninfected. A variety of mechanisms potentially able to confer resistance to HIV infection, including cell-mediated and (unconventional) humoral immune responses, as well as mutations affecting receptors for virus entry have been considered and analysed. In this article, we want to discuss recent reports on specific immune responses and genetic factors potentially involved in mechanisms of protection, and to present some of our data relative to a cohort of people sexually exposed to HIV-1, but persistently seronegative. These EU (exposed uninfected) individuals can be distinguished from "normal" unexposed controls on the basis of significantly increased frequencies of a number of immunological parameters that might be considered "unconventional" correlates of HIV infection/protection. However, EU individuals are highly heterogeneous since the various unconventional immune responses considered can be present in all possible combinations. Aim of future research will be to ascertain the role of such immune responses in the maintenance of the protection state, or their secondary nature as signals of a particular kind of infection.

Genetic Variation↗
PubMedDate not supplied

Soluble CD30, tumour necrosis factor (TNF)-alpha, and TNF receptors in primary HIV-1 infection: relationship with HIV-1, RNA, clinical outcome and early antiviral therapy.

The natural course of human immunodeficiency type 1 (HIV-1) infection varies considerably. The identification of laboratory disease markers has become critically important to patient management. This study, carried out on 37 patients with primary HIV-1 infection (PHI), shows that, along with plasma HIV-1 RNA and CD4+ T cell counts, evaluation of plasma levels of some immune activation markers (sCD30, TNF-alpha, and sTNFR-I) may help to identify patients at risk of a more rapid disease progression, suggesting that immune activation is among the factors who determine the rate of disease progression. Early combination antiviral therapy significantly decreased levels of virus load and of immune activation markers, suggesting that it may reduce the extent of immune activation through the suppression of HIV-1 replication. Among others, sCD30 could be a more sensitive marker of immune activation, and it might be also useful in the monitoring of the response to antiviral therapy.

Anti-HIV Agents↗