COVID-19 among healthcare workers in a specialist infectious diseases setting in Naples, Southern Italy: results of a cross-sectional surveillance study.

A coronavirus disease 2019 (COVID-19) surveillance study was performed in March-April 2020 among asymptomatic healthcare workers (HCWs) at a specialist infectious diseases hospital in Naples, Italy. All HCWs underwent two rounds of molecular and serological testing for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). One hundred and fifteen HCWs were tested; of these, two cases of infection were identified by reverse transcriptase polymerase chain reaction and two HCWs were SARS-CoV-2 immunoglobulin G seropositive. The overall prevalence of current or probable previous infection was 3.4%. The infection rate among HCWs was reasonably low. Most of the infected HCWs had been asymptomatic for the preceding 30 days, which supports the need for periodic screening of HCWs for COVID-19.

Rapid virological response in peripheral blood mononuclear cells with an increase of hepatitis C virus-specific interferon-gamma production predisposes to sustained virological response in patients with chronic hepatitis C genotype 1 undergoing treatment with pegylated-interferon alpha 2a plus ribavirin.

OBJECTIVE: Viral load evaluation in plasma, after 1 month of treatment, represents one of the most important parameters to predict treatment response during interferon (IFN) treatment in chronic hepatitis C (CHC). It has been proven that hepatitis C virus (HCV) RNA may be present in peripheral blood mononuclear cells (PBMCs) but few studies have investigated the viral load in PBMCs during treatment. The aim of this study was to evaluate HCV RNA in PBMCs during therapy with pegylated-IFN-alpha2a plus ribavirin and whether its clearance in PBMCs may induce a treatment response. Furthermore, we also analyzed the IFN-gamma and interleukin (IL)-4 responses of PBMCs during therapy. MATERIAL AND METHODS: We studied 35 patients with CHC genotype 1 undergoing antiviral treatment with pegylated IFN-alpha2a 180 microg weekly plus ribavirin 1000 mg/daily. In these patients we evaluated HCV-RNA in plasma and PBMCs, IFN-gamma and IL-4 before treatment, after 1, 3 and 12 months of treatment and 6 months after the end of treatment. RESULTS: We found that rapid virological clearance of HCV-RNA in PBMCs with a restored and improved HCV-specific IFN-gamma response was statistically significantly higher in those with a sustained virological response (SVR). CONCLUSION: Patients having a rapid virological response in PBMCs with an improved Th1 network achieve a complete SVR, whereas those having viral clearance only in plasma without a restored Th1 network have a relapse.

Fosamprenavir treatment in a highly active antiretroviral therapy schedule induces a HCV-RNA decrease and a Th1 network boost in HIV/HCV-coinfected patients.

HIV/HCV co-infected naïve patients (four females and six males) were evaluated for their response to the following treatment schedule: [(AZT 300 mg + 3TC 300 mg twice daily) + (fosamprenavir 700 mg twice daily) + (RTV 100 mg)]. CD3+/CD4+ T cells, interferon-gamma (INF-gamma) and interleukin-4 (IL-4) HCV-specific response, viral loads and transaminase levels were evaluated at time 0, and after 1, 3 and 6 months of therapy (T0, T1, T3, and T6 respectively). HIV-RNA, HCV-RNA and transaminases decreased at T1 and T3 compared with T0 (Mann-Whitney p <0.001, p <0.01 and p <0.01, respectively). At all time points, CD4+ and HCV-specific INF-gamma responses were higher (p <0.001; p <0.001), and IL-4 lower (p <0.01) after treatment. At T6, HCV-RNA was only negative in four out of ten patients whereas all had normal transaminase levels. These findings indicate that HAART treatment including fosamprenavir is able to activate a Th1 network in HIV/HCV co-infected patients. Moreover, these results, to be confirmed by larger cohort follow-up studies, suggest that this protease inhibitor could have potential implications for the treatment of chronic hepatitis C in HIV-positive patients.

Elevated CD4+/CD25+ T-cell frequency and function during hepatitis C virus recurrence after liver transplantation.

BACKGROUND/AIM: Factors involved in hepatitis C virus (HCV) recurrence versus acute cellular rejection are not fully understood. The aim of the present study was to investigate whether patients with recurrence after liver transplantation (OLT) showed similar CD4(+)/CD25(+) cell frequency and function as those who became chronically infected. PATIENTS AND METHODS: After written informed consent, we enrolled 20 patients (group A) who underwent OLT with HCV recurrence within 6 months. HCV-RNA and hypertransaminasemia were used to assess the reactivation of viral hepatitis. CD4(+)/CD25(+) T cells were enumerated using a flow cytometry assay, gated on CD3 cells, stained for FoxP3. After immunomagnetic sorting (Dynal, Oslo, NW), Treg suppressor activity was measured, as the ability to inhibit proliferation of autologous CD4(+)/CD25(-) T cells (anti-CD3/CD28 stimulation-1:2, 1:20 ratio). Eight patients with acute hepatitis C who evolved to a chronic infection after 6 months (group B) were used as positive controls, while 10 healthy individuals were negative controls (group C). RESULTS: We did not observe any difference in CD4(+)/CD25(+) frequency or function among group A compared with group B (CD4(+)/CD25(+) = 14% +/- 2% versus CD4(+)/CD25(+) = 16% +/- 3%), although both groups were significantly increased with respect to group A (CD4(+)/CD25(+) = 6% +/- 3%; Mann-Whitney U test, P < .01). CONCLUSION: Patients developing HCV recurrence after OLT have the same immunoregulatory network as patients with acute hepatitis C evolving to persistent infection, likely suggesting that CD4(+)/CD25(+) numbers may be a marker to predict recurrence of HCV after OLT.

Acute rejection after liver transplantation: Is there a specific immunological pattern?

The aim of the study was to assess various T-cell subsets and cytokine secretion patterns both in liver tissue and in the peripheral blood of 24 liver transplant patients to assess possible specific immunological involvement in early acute rejection episodes after liver transplantation. Particularly, we studied CD4+ CD7+, CD8+ CD38+, and CD4+ CD25+ T cells by flow cytometry, as well as contemporaneously, interleukin (IL)-2 and IL-10 secretion by ELISpot to determine possible Th1-like immune responses and the immunomodulation expressed by Treg cells in acute liver rejection, respectively. As a control group we included patients transplanted without acute rejection. Early acute rejection within the first 4 weeks was proven histologically in 42% of patients. It was associated with a greater expression of CD4+ CD7+ and CD8+ CD38+ T cells in the liver than in the blood (P < .001). A contemporaneous reduced expansion of liver Treg cells was evident in patients with acute rejection (P < .001). Our data suggested that a preferential Th1-like immune mechanism operated in local fashion as characterized by a decreased presence in the liver and blood of Treg cells.