104 research outputs found
Residual risk of transfusion-transmitted HCV and HIV infection by antibody-screened blood in Italy
No full textBACKGROUND: This study was designed to assess the risk of transmitting HCV and HIV by transfusion of antibody-screened blood and to estimate the additional reduction in risk that may be achieved through the implementation of direct viral detection assays in Italy. STUDY DESIGN AND METHODS: Clinical and laboratory data of 2,411,800 blood donations collected from repeat volunteer donors from 1996 through 2000 were analyzed. The risk of transmitting HCV or HIV from screened blood donated during the window period was estimated using a mathematical model. RESULTS: The residual risk of donating antibody-negative infectious blood was estimated at 1 in 127,000 donations for HCV and 1 in 435,000 for HIV. The use of NAT should further reduce such risk by 83 percent for HCV and 50 percent for HIV. CONCLUSION: The residual risk of HCV or HIV transmission through screened blood is currently very small in Italy. The implementation of direct viral detection assays can further improve the safety of blood supply
Transfusion of red blood cells from an HIV-RNA-positive/anti-HIV-negative donor without HIV infection in the recipient
No full textMore than 90 percent of recipients of HIV-1-containing blood components acquire HIV infection.1 We report the case of a recipient of red blood cells (RBCs), collected from an HIV-1-infected donor in the HIV-RNA positive/anti-HIV negative window phase, who did not develop HIV infection.
In September 2004, HIV-1-specific antibodies(HIV1-2 Ab-Capture EIA, Ortho Diagnostic System,Raritan, NJ) and p24 antigen (Genescreen Plus HIV Ag-Ab,
Bio-Rad Laboratories, Hercules, CA) were detected in a 44-year-old male blood donor who denied HIV-related risk behavior. The HIV-RNA assay (Cobas Amplicor HIV-1 Monitor Test, v. 1.5, Roche Diagnostics, Indianapolis, IA)confirmed HIV infection (56,000 copies/ml). Viral genotyping(AbbottViroseqTM HIV1 Genotyping SystemVersion
2.0, Abbott Molecular, Des Plaines, IL) showed an HIV-1 subtype B virus, not resistant to anti-retroviral medications.
A routine blood donation 6 months earlier tested
anti-HIV-negative. At that time, nucleic acid testing (NAT)for HIV was not performed in our Blood Service, and the components were released for transfusion. The RBCs were transfused 7 days after collection to the patient of this report. The plasma was transferred for processing(Kedrion, Lucca, Italy). Retrospectively, a sample that had
been retained from this donation tested positive for HIVRNA(98 copies/mL). However, a sample retained from a blood donation on December 22, 2003, tested repeatedly HIV-RNA negative. Notice of the HIV-infected plasma unit was communicated immediately to Kedrion and to the recipient, a 54-year-old woman who had laparoscopic surgery. She has remained negative for HIV–RNA, p24Ag and anti-HIV when tested at 6, 12, and 14 months after transfusion.
In vitro studies showed that the recipient’s peripheral blood mononuclear cells (PBMCs) could be infected with the donor’s HIV isolate. The recipient was genotyped by PCR as wild-type CCR5. Because exposure to HIV in the absence of seroconversion can be inferred by the detection
of HIV-specific T lymphocytes,2,3 an in-depth immunologic analysis on the recipient was performed 14 months after the RBCs transfusion.
Recipient’s PBMCs were stimulated with pools of antigens from env and gag regions of HIV. A higher than normal percentage of env-specific, IL-2-expressing CD4+ T lymphocytes (0.9%) was observed, whereas neither envspecific CD8+ nor gag-specific CD4+ or CD8+ T lymphocytes were detected. Naïve (CCR7+/CD45RA+), as well as central (CCR7+/CD45RA-) and effector (CCR7-/CD45RA-)memory CD4+ and CD8+ T lymphocytes, were measured.
Both CD4+ and CD8+ naïve lymphocytes were reduced(11.3% vs. 23.4% and 10.1% vs. 22.2%) whereas CD8+ terminally-differentiated lymphocytes were augmented(22.7% vs. 7.0%) compared to results obtained in sex- and age-matched controls.
These results strongly suggest that exposure to HIV
antigens in the absence of replicating virus occurred in this patient. Thus, only actual infection with live and replicating virus would result in presentation of viral antigens in association with HLA class Imolecules, and elicitation of a CD8-mediated immune response. Additionally, responses to env, but not to gag, would be detected in the case of exposure toviral antigens in the absence of viral replication within the host cells. Finally, the observation that naïve cells were decreased in this patient is suggestive of a massive antigenic exposure, possibly HIV antigen-driven.
Of importance, the donor’s HIV isolate was able to infect the recipient’s PBMCs and a CCR5D32 deletion was not present in either the donor or the recipient.
Other investigators have reported cases illustrating that blood components may differ in their ability to transmit HIV infection.1,4 In one report, platelets from an HIVpositive donor transmitted infection, while RBCs from the same blood collection did not.5 There are several possible explanations for exposure to HIV without infection,including: 1) the presence of a low viral load at the time of donation; 2) a sub-infective volume of plasma in the RBCs; 3) loss of infectivity during storage of the component before transfusion; and 4) recipient’s resistance related to genetic background (other than the CCR5D32 deletion,which was not present in our patient).
We believe that our results indicate that the presence of a strong cell-mediated immune response, possibly secondary to the exposure to a low amount of HIV, plays a role in resistance to HIV infection
Response to “Questions arising on phlebotomy in polycythemia vera: prophylactic measures to reduce thromboembolic events require patient-focused decisions” by Heidel et al
No full textTen years since the last Chikungunya virus outbreak in Italy. History repeats itself
No full textThe prevalence of Arbovirus (arthropod-borne virus) infections is increasing worldwide. Recently, new clusters of autochthonous cases have been reported in countries with temperate climates where the competent vector is present. This scenario represents a new threat for transfusion medicine.CHIKV has been a significant public health concern in Asian and African countries, where most epidemics occurred in the 1960s and 1990s, and is newly emerging in Middle East, Pacific, American, and European countries. Exactly 10 years after the first European outbreak of CHIKV, the virus has emerged again in Italy where the competent vector (Aedes albopictus) is present
Human vascular wall mesenchymal stromal cells contribute to abdominal aortic aneurysm pathogenesis through an impaired immunomodulatory activity and increased levels of matrix metalloproteinase-9
No full textBackground: The main histopathological features of abdominal aortic aneurysm (AAA) are tissue proteolysis mediated by matrix metalloproteinases (MMPs) and inflammation. This study aimed at verifying the presence and contribution of mesenchymal stromal cells (MSCs) to aneurysmal tissue remodeling. Methods and Results: MSCs were successfully isolated from the AAA wall of 12 male patients and were found to express mesenchymal and stemness markers. MMP-2/-9 are involved in AAA progression and their mRNA levels in AAA-MSCs resulted higher than healthy MSCs (cMSCs), especially MMP-9 (400-fold increased). Moreover, MMP-9 protein and activity were pronounced in AAA-MSCs. Immunomodulation was tested in AAA-MSCs after coculture with activated peripheral blood mononuclear cells (PBMCs) and revealed a weak immunosuppressive action on PBMC proliferation (bromodeoxyuridine incorporation, flow cytometry assay), together with a reduced expression of anti-inflammatory molecules (HLA-G, IL-10) by AAA-MSCs compared to cMSCs. MMP-9 expression in AAA-MSCs was shown to be negatively modulated under the influence of cMSCs and exogenous IL-10. Conclusions: MSCs with stemness properties are niched in human AAA tissues and display a dysregulation of functional activities; that is, upregulation of MMP-9 and ineffective immunomodulatory capacity, which are crucial in the AAA progression; the possibility to modulate the increased MMP-9 expression by healthy MSCs and IL-10 suggests that novel therapeutic strategies are possible for slowing down AAA progression
The expert in hemostasis and thrombosis in the italian health system: Role and requirements for a specific clinical and laboratory expertise
No full textSummary Hemorrhagic and thrombotic diseases are very heterogeneous and may affect a relevant part of the population, as in the case of patients taking antithrombotic drugs. The appropriate management of such conditions requires the availability of specific diagnostic assays, together with knowledge of the possible clinical syndromes and of their appropriate treatment. This could be achieved only through qualified clinical expertise and specialized labs supervised by trained personnel. Such a diagnostic and therapeutic organization is not widely available in Italy but for a limited number of major hospitals. Extending the availability of such resources would berelevant for patients and cost-effective for the National Health System. This document, promoted by SISET and by allied Scientific Societiesin 2012, is aimed at identifying the level of scientific and professional expertise required to define a physician as an Hemostasis and Thrombosis Expert. The increasing levels of expertise required as the organizative settings became more complex and comprehensive as delineated
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