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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Viral infections during pregnancy may cause fetal or neonatal damage. Clinical intervention, which is required for certain viral infections, relies on laboratory tests performed during pregnancy and at the neonatal stage. This review describes traditional and advanced laboratory approaches and testing methods used for assessment of the six most significant viral infections during pregnancy: rubella virus (RV), cytomegalovirus (CMV), varicella-zoster virus (VZV), herpes simplex virus (HSV), parvovirus B19 and human immunodeficiency virus (HIV). Interpretation of the laboratory tests results according to studies published in recent years is discussed.
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PMID:Laboratory assessment and diagnosis of congenital viral infections: Rubella, cytomegalovirus (CMV), varicella-zoster virus (VZV), herpes simplex virus (HSV), parvovirus B19 and human immunodeficiency virus (HIV). 1656 72

Many viruses can be responsible for systemic vasculitis, the most frequent being hepatitis B virus-related polyarteritis nodosa (HBV-PAN), even though its incidence has decreased over the past few decades. Mixed cryoglobulinemia has been shown to be associated with hepatitis C virus (HCV) infection in more than 80% of the patients, but it remains asymptomatic in most of them with only a minority developing vasculitis. Human immunodeficiency virus (HIV), erythrovirus B19, cytomegalovirus, varicella-zoster virus and human T-cell lymphotropic virus (HTLV)-1 have also been reported to be associated with or implicated in the development of vasculitides. On the other hand, some bacteria, fungi or parasites can also cause vasculitis, mainly by direct invasion of blood vessels or septic embolization, leading, e.g., to the well-known feature of 'mycotic aneurysm'. Syphilitic aortitis and/or cerebrovascular disease and rickettsial diseases are other, more specific, bacteria-induced vasculitides. Recognizing an infectious origin of vasculitides is of great importance because treatment strategies differ from those applied to non-infectious forms. Effective antimicrobial drugs are mandatory to treat bacterial, parasitic or fungal infections, while the combination of antiviral agents and plasma exchanges has been proven to be effective against HBV-PAN. This latter strategy might also be effective against HIV-associated vasculitis and, unlike cytotoxic agents, does not jeopardize the outcome of HIV-infected patients. In the context of HCV-related cryoglobulinemic vasculitis, antiviral drugs are necessary to achieve recovery, in combination with low-dose corticosteroids and/or rituximab. In the near future, newer antiviral agents will probably also have their place in the therapeutic armamentarium for these patients.
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PMID:Vasculitides secondary to infections. 1685

Transplantation-associated infections are caused by an infected transplanted organ or the endogenic or exogenic environment of the recipient in a state of induced immunodeficiency. The best therapy would be to reconstitute the immunodeficiency, but this is usually impossible as it endangers the transplanted organ. Thus, a specific, standardised anti-infectious therapy is needed even in the absence of clearly identified micro-organisms [bacteria (in two thirds gram-positive rods), parasites (in central Europe predominantly Toxoplasma), fungi (especially Candida spp. or Aspergillus spp.) or viruses (such as Parvovirus B19 and Cytomegalovirus)]. Origins of infection (e.g., hygiene), types of infection (e.g., reactivation), typical localisations, diagnostic tools (e.g., blood cultures, antigenic tests, PCR, CT, advantages and disadvantages of antibody assays) and possible therapies are briefly discussed. The take home messages are to avoid economy measures in microbial diagnostics and to use CMV-seronegative donors whenever possible.
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PMID:[Transplantation-associated infections]. 1689 37

Following the devastating effects of blood-transmitted human immunodeficiency virus (HIV), blood establishments have become increasingly vigilant for the emergence or re-emergence of new threats to the safety of the blood supply. Many agents have fulfilled the broad definition of emerging blood-transmitted infections, including West Nile virus (WNV), Trypanosoma cruzi, Plasmodium spp., Babesia spp., parvovirus B19, dengue virus, and the prions that cause variant Creutzfeld-Jacob disease (vCJD). Other agents such as human herpes virus-8 (HHV-8-Kaposi's sarcoma virus) and Borellia (Lyme disease) and, perhaps, avian flu virus, are known to have a viremic phase, but have not yet been proved to be transfusion-transmitted. In the wake of these threats, transfusion services use a variety of donor screening interventions, including serologic assays, nucleic acid assays, and geographic exclusions based on potential exposure. The ultimate safeguard may be a pre-emptive pathogen inactivation strategy that will disrupt all nucleic acid-containing agents (though not prions). Considerable effort and resources have been invested in this arena, but currently no single technique is effective for inactivation of both liquid and cellular blood products and toxicity issues have not been completely resolved. The blood supply is remarkably safe with the risk of major pathogens such as hepatitis C virus (HCV) and HIV now reduced to less than one transmission per 2 to 3 million exposures. However, to approach near-zero infectious disease risk for emerging and re-emerging pathogens, new strategies such as pathogen inactivation or multi-pathogen microarray technology will need to be developed or refined.
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PMID:Emerging infectious diseases that threaten the blood supply. 1719 45

The aim of this study was to characterize the proinflammatory and T helper (Th)1/Th2 cytokine responses during acute parvovirus B19 (B19) infection and determine whether an imbalance of the Th1/Th2 cytokine pattern is related to persistent B19 infection. Cytokines were quantified by multiplex beads immunoassay in serum from B19-infected patients and controls. The cytokine responses were correlated with B19 serology, quantitative B19 DNA levels and clinical symptoms. In addition to a proinflammatory response, elevated levels of the Th1 type of cytokines interleukin (IL)-2, IL-12 and IL-15 were evident at time of the initial peak of B19 viral load in a few patients during acute infection. This pattern was seen in the absence of an interferon (IFN)-gamma response. During follow-up (20-130 weeks post-acute infection) some of these patients had a sustained Th1 cytokine response. The Th1 cytokine response correlated with the previously identified sustained CD8+ T cell response and viraemia. A cross-sectional study on patients with persistent B19 infection showed no apparent imbalance of their cytokine pattern, except for an elevated level of IFN-gamma response. No general immunodeficiency was diagnosed as an explanation for the viral persistence in this later group. Neither the acutely infected nor the persistently infected patients demonstrated a Th2 cytokine response. In conclusion, the acutely infected patients demonstrated a sustained Th1 cytokine response whereas the persistently infected patients did not exhibit an apparent imbalance of their cytokine pattern except for an elevated IFN-gamma response.
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PMID:Cytokine responses in acute and persistent human parvovirus B19 infection. 1730 90

Although most persons with parvovirus B19 infection are asymptomatic or have mild, nonspecific, cold-like symptoms, several clinical conditions have been linked to the virus. Parvovirus B19 usually infects children and causes the classic "slapped-cheek" rash of erythema infectiosum (fifth disease). The virus is highly infectious and spreads mainly through respiratory droplets. By the time the rash appears, the virus is no longer infectious. The virus also may cause acute or persistent arthropathy and papular, purpuric eruptions on the hands and feet ("gloves and socks" syndrome) in adults. Parvovirus B19 infection can trigger an acute cessation of red blood cell production, causing transient aplastic crisis, chronic red cell aplasia, hydrops fetalis, or congenital anemia. This is even more likely in patients with illnesses that have already shortened the lifespan of erythrocytes (e.g., iron deficiency anemia, human immunodeficiency virus, sickle cell disease, thalassemia, spherocytosis). A clinical diagnosis can be made without laboratory confirmation if erythema infectiosum is present. If laboratory confirmation is needed, serum immunoglobulin M testing is recommended for immunocompetent patients; viral DNA testing is recommended for patients in aplastic crisis and for those who are immunocompromised. Treatment is usually supportive, although some patients may require transfusions or intravenous immune globulin therapy. Most patients recover completely.
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PMID:Clinical presentations of parvovirus B19 infection. 1730 69

CD40 ligand (CD40L) deficiency is an X-linked combined immunodeficiency characterized by impaired class switch recombination. We analyzed clinical and molecular findings in 11 Argentinian patients from seven unrelated families. The mean age at onset of symptoms was 1.1 years (0.5-3.0 years) and the 10 alive patients have a median age of 17 years. We identified two nonsense mutations, including R11X reported as a "hypomorphic" defect, four missense mutations, and one point deletion. Although R11X was associated herein with parvovirus B19-anemia and higher Igs levels as previously described, histoplasmosis and Pneumocystis jiroveci pneumonia were also present. Other so-called "milder" mutation, T254M, was present in three related patients clinically and immunologically undistinguishable from the rest of the cohort. Furthermore, 10 of the 11 patients, having heterogeneous mutations, never had persistent neutropenia, none presented Cryptosporidium sp. infection nor developed liver-biliary tract disease, highlighting the debatable concept of "milder" mutations.
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PMID:Clinical follow-up of 11 Argentinian CD40L-deficient patients with 7 unique mutations including the so-called "milder" mutants. 1735 59

Erythrovirus (parvovirus) B19 (B19) is a common human pathogen. It is a non-enveloped single-strand DNA virus packaging its genome in small tight capsids consisting of viral VP1 and VP2 proteins. It is now accepted that B19 is a relatively quickly evolving virus having diverged in several genetic variants recently identified. The main route of B19 transmission is respiratory, with a majority of infections occurring during childhood and manifesting as erythema infectiousum. B19 can also be transmitted vertically and via blood transfusion and organ transplantation. The majority of adult populations show immunological evidence of previous exposure to B19. Although the immune response is able to clear infection and provide life-long protection against B19, recent data suggest that in some, if not the majority, of individuals the acute phase of infection is followed by viral persistence in the blood or other tissues regardless of the host's immunocompetence. Transmission of B19 by blood and blood products and its resistance to common viral inactivation methods raises several blood safety questions, still unanswered. The diversity of B19 strains and the ability of the virus to persist in the presence of specific antibodies raise the issue of transmissibility by transfusion not so much to immunocompetent recipients but rather to the large proportion of recipients in whom there is some degree of immunodeficiency. The ability of the virus to reactivate in immunodeficient recipients may create difficulties in differentiating between transfusion transmission and reactivation.
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PMID:Human erythrovirus B19 and blood transfusion - an update. 1768 Sep 52

We describe a 26-year-old female referred to us because of recurrent bacterial pneumonia. Her immunoglobulin profile on admission was; IgG 1920 mg/l, IgA 60 mg/l, IgM 260 mg/l, IgD below 20 mg/l, IgE below 1 kU/l. Antinuclear antibodies, EBV VCA IgM, anti-parvovirus B19 IgM antibodies and hepatitis infection markers were all negative. Bone marrow aspiration revealed normal cellularity without abnormal cells, especially plasma cell proliferation. No rearrangement for IgH and TCR was observed as determined by Southern blot analysis. By the given data, a diagnosis of common variable immunodeficiency (CVID) was made. The genesis of this disease remained unclear. In this study, proliferation and immunoglobulin production with or without several stimulators were examined. Proliferation stimulated by PHA, Con-A, LPS, or IL-2 was decreased compared to that of healthy individuals. Immunoglobulin production after stimulation with several agents was quite low. Interestingly, however, IL-2 or IL-4 could increase IgM production on 6 days culture significantly. These results indicate that IL-2 or IL-4 possibly restore T cell responses to several antigens and induce B cell differentiation.
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PMID:Partial restoration of immunoglobulin production by cytokines in common variable immunodeficiency. 1782 53

Symptomatic manifestations of parvovirus B19 infection range from harmless conditions such as 5th disease of the child or arthropathy of the middle-aged woman to life threatening disease such as transient aplastic crisis during sickle cell disease, chronic anaemia in immunodeficiency states or hydrops foetalis during pregnancy. Increasing knowledge of parvovirus B19 has led to a better understanding about how a single and unvariant erythrovirus causes such a variety of diseases. The importance of age, hematopoietic and immune status has been raised and besides, effective diagnostic assays, treatments and possibly vaccine have been developed that can be rationally used at the light of this knowledge.
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PMID:[Parvovirus B19: importance of diathesis in the clinical expression of a common infection]. 1784 96


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