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This paper provides a recent legal case which calls into discussion the women’s safe access to voluntary termination of pregnancy (VTP) after the first 90 days. On 15 January 2021, the Italian Supreme Court sentenced a physician to damage compensation because he did not correctly inform the patient, in her 22nd week of pregnancy, about the risks to the fetus relating to an infection from cytomegalovirus (CMV). The option for VTP was not offered since, at the time of the woman’s request, medical investigations did not show the evidence of fetal malformations, neither there were concrete risks for the life of the mother, as Italian law requires. The baby was born with severe brain injuries. The case is noteworthy because it offers a new precedent to extend legal requirements for late VTP. The impact of this decision must be tested in the clinical practice. Further studies are necessary to evaluate possible law amendments extending access conditions for this practice and new policies promoting the strengthening of informative and assistance procedures, including psychological help, to the pregnant woman are needed, as well.

Background: Acute coronary syndromes (ACS) are a major cause of morbidity and mortality. As cytomegalovirus (CMV) may contribute to Cardio-Vascular (CV) manifestations, we sought to provide a proof-of-concept for the involvement of coronary and/or systemic CMV-reactivation as a possible ACS trigger. Methods: We prospectively enrolled consecutive patients undergoing a coronary angiography for ACS (acute-cases, N=136), or non-ACS reasons (chronic-cases, N=57). Matched coronary and peripheral blood-samples were processed for quantification of CMV-DNAemia (RT-PCR), CMVIgG/ IgM, and CMV-IgG avidity (ELISA). Peripheral-blood samples from 17 healthy subjects were included as controls. Results: Out of the 193 cases included, 18.1% were aged ≤55 years, 92.5% were Central-European, and 100% immunocompetent. CMV-IgG seroprevalence was 91.7% (95%CI: 87.8-95.6), significantly higher than in healthy-controls (52.9% [95%CI: 29.2-76.5]; p

Anyplex™II HPV28 is a new PCR assay designed for HPV genotyping. It can detect 28 HPV types including 19 high-risk and 9 low-risk types. This study evaluated the performance of Anyplex™II HPV28 on 123 fresh cervical samples screened in parallel with HPV Sign® Genotyping Test. Of the 123 samples screened, 93 were positive, 15 negative, and 15 discordant. The total number of HPV positive samples combined was 108: 38 single infections and 70 multiple infections. The agreement between the two tests was 87.8%, κ=0.592. Genotype specific agreement was strong for HPV 16 (k=0.761), HPV 18 (k=0.674), and HPV 35 (k=0.796). Sensitivity and specificity of Anyplex™II HPV28 assay using HPV Sign® Genotyping Test as reference was 84.8% and 94%; conversely, sensitivity and specificity of HPV Sign® Genotyping Test was 29% and 99.5%. Anyplex™II HPV28 assay is a sensitive and specific assay suitable for HPV genotyping but requires clinical validation.

During the spring of 2009, a new influenza A (H1N1) virus of swine origin emerged and spread worldwide causing a pandemic influenza. Here, 329 naso-pharyngeal swabs collected from patients with flu-like symptoms were analyzed by real-time PCR for the presence of H1N1 2009 pandemic virus. Twenty-five samples collected from immunocompetent and immunodepressed patients contained the H1N1 pandemic virus. Phylogenetic analysis of the hemagglutinin and neuraminidase genes showed no obvious differences in terms of similarity and/or homology between the sequences identified in immunocompetent individuals and those obtained from immunocompromised patients. Pre-existing clinical conditions may influence the outcome of H1N1 disease.

Objective To investigate lamivudine (LAM)-resistance profiles of hepatitis B virus (HBV) at the early stages of virological breakthrough (serum HBV-DNA 12–345 IU/ml) or when HBV-DNA is undetectable. Methods Sixty-four HBV-mono-infected patients were enrolled: 25 had virological breakthrough with serum HBV-DNA ranging from 12 to 345 IU/ml during first-line LAM-monotherapy; 24 were on LAM-monotherapy, and 15 were on LAM + adefovir dipivoxil (ADV) with undetectable serum HBV-DNA ( Results HBV-reverse transcriptase was successfully sequenced in 22 (88.0%) LAM-treated patients with HBV-DNA between 12 and 345 IU/ml, and in 12 (30.8%) patients receiving LAM (±ADV) with HBV-DNA Drug-resistance mutations were observed in 17 (77.2%) LAM-treated patients with virological breakthrough: 8 M204V, 7 M204I, 1 M204I/V, and 1 A181T. One or ≥2 compensatory mutations were found in 10 (58.8%) and in 4 (23.5%) patients. Drug-resistance mutations were present also in patients with undetectable serum HBV-DNA: M204I was detected in 2 patients receiving LAM-monotherapy, and V84M in 1 patient receiving LAM + ADV. Conclusion Overall findings support the existence of drug-resistance mutations even at very low levels of viral replication. The persistence of low-level HBV replication and consequent drug-resistance emergence should be considered when choosing therapeutic strategies.

Genotype determination is recommended before starting anti-HCV therapy to determine the duration of treatment (PEG-Interferon+ribavirin). The Versant HCV Genotype 2.0 assay, based on the reverse hybridization of the 5'UTR segment and core region of hepatitis C virus (HCV), has been one of the assays used most widely for HCV genotyping. A multicenter evaluation of the more automated Abbott RealTime HCV Genotype II assay was carried out on 124 HCV positive sera tested previously with the Versant HCV Genotype 2.0 assay. There was good agreement between the two assays. Type concordance was 95.9% (117/122) while concordance at the subtype level for genotype 1 was 95.6% (43/45). The Abbott RealTime HCV Genotype II assay is automated, allowing a substantial reduction of time-to results and hands-on time. The combined features of full automation, objective interpretation and digital archiving make this assay useful in a diagnostic setting.

The new Abbott RealTime hepatitis B virus (HBV) assay was compared to the Cobas AmpliPrep/Cobas TaqMan assay with 128 serum samples from patients with chronic hepatitis B. There was an excellent correlation (r= 0.961) between the two assays, with the Abbott RealTime test showing at least equivalent sensitivity and a slightly wider dynamic range than the Cobas TaqMan assay. By coupling high sensitivity with a large dynamic range, the Abbott RealTime HBV assay is useful in monitoring the response to antiviral therapy.

Background Storage and shipment conditions of clinical specimens affect the quality of nucleic acids and may interfere with molecular analysis. The aim of our study was to verify whether blood storage at room temperature affects single nucleotide polymorphisms analysis; moreover, we analysed the consequences of serum storage at 4°C on viral load determination of hepatitis B and C viruses. Methods For single nucleotide polymorphism screening, genomic DNA was extracted from EDTA whole blood samples stored at room temperature for different times, quantified photometrically, and Factor V Leiden point mutation analysis was performed. For viral load determination, serum samples with medium or low viremias were stored at +4°C for different times and analysed by Cobas AmpliPrep/Cobas TaqMan tests for hepatitis B virus (HBV) DNA or hepatitis C virus (HCV) RNA. Results While mutation analysis was successfully performed on all samples tested, serum storage at +4°C of HBV- and HCV-infected sera decreased viral load, in particular for low viremias. Conclusions Storage of blood samples at room temperature up to 1 month does not affect the feasibility of genetic analysis, while serum storage at +4°C affects viral load.

Objectives: The aim of this study was to investigate the development and progression of phenotypic resistance to the HIV-1-reverse transcriptase (RT) inhibitor lamivudine, and genotypic variations of HIV-1-RT occurring under lamivudine treatment in HIV-1-infected human primary monocytes-macrophages (M/M). Methods: Cellular passages in the presence of lamivudine were performed every 2 weeks by transferring supernatants of infected M/M to fresh M/M. A fitness assay using wild-type virus and a lamivudine-resistant HIV-1 virus (harbouring the M184V RT mutation) was performed in peripheral blood mononuclear cells. Culture supernatants were tested for p24 antigen production and RT activity. The M184V RT mutant virus was obtained by site-directed mutagenesis on a CCR5-using HIV-1 backbone. Results: The mutagenized M184V RT virus showed full resistance to lamivudine in M/M. However, no detectable phenotypic and genotypic resistance (neither virus breakthrough, nor RT resistance-related mutations) developed in M/M infected by HIV-1 and cultured for up to seven passages in vitro (i.e. 105 days). This inefficiency of M/M to develop M184V RT mutated virus is tightly related to the low 2'-deoxynucleotide (dNTP) pool in such cells, which in turn decreases the kinetics of HIV-1-RT. Despite this, the M184V RT mutant virus replicates in M/M, although with a 30% decreased efficiency compared with the wild-type. Conclusions: Our results show that the chances of development of resistance are far lower in M/M than in lymphocytes. This underlines the importance and the peculiar role of M/M as reservoirs of either wild-type or resistant strains in human organs.