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Biomedical subjects

Jan Andersson

Publications and source records attributed to Jan Andersson.

18 recordsLinked to original sources

Antioxidant intake, plasma antioxidants and oxidative stress in a randomized, controlled, parallel, Mediterranean dietary intervention study on patients with rheumatoid arthritis.

BACKGROUND: Previously we have reported that patients with rheumatoid arthritis (RA) obtained a significant reduction in disease activity by adopting a Mediterranean-type diet. The present study was carried out to investigate the antioxidant intake, the plasma levels of antioxidants and a marker of oxidative stress (malondialdehyde) during the study presented earlier. METHODS: RA patients randomized to either a Mediterranean type diet (MD group; n = 26) or a control diet (CD group; n = 25) were compared during a three month dietary intervention study. Their antioxidant intake was assessed by means of diet history interviews and their intake of antioxidant-rich foods by a self-administered questionnaire. The plasma levels of retinol, antioxidants (alpha- and gamma-tocopherol, beta-carotene, lycopene, vitamin C and uric acid) and urinary malondialdehyde (MDA), a marker for oxidative stress, were determined using high performance liquid chromatography. The Student's t-test for independent samples and paired samples were used to test differences between and within groups. For variables with skewed distributions Mann-Whitney U-test and Wilcoxon signed ranks test were performed. To evaluate associations between dietary intake of antioxidants, as well as between disease activity, MDA and antioxidants we used Pearson's product moment correlation or Spearman's rank correlation. RESULTS: The MD group had significantly higher intake frequencies of antioxidant-rich foods, and also higher intakes of vitamin C (p = 0.014), vitamin E (p = 0.007) and selenium (p = 0.004), and a lower intake of retinol (p = 0.049), compared to the CD group. However, the difference between the groups regarding vitamin C intake was not significant when under- and over-reporters were excluded (p = 0.066). There were no changes in urine MDA or in the plasma levels of antioxidants (after p-lipid adjustments of the tocopherol results), from baseline to the end of the study. The levels of retinol, vitamin C and uric acid were negatively correlated to disease activity variables. No correlation was found between antioxidant intake and the plasma levels of antioxidants. CONCLUSIONS: Despite an increase in reported consumption of antioxidant-rich foods during the Mediterranean diet intervention, the levels of plasma antioxidants and urine MDA did not change. However, the plasma levels of vitamin C, retinol and uric acid were inversely correlated to variables related to RA disease activity.

Clinical Trial↗

Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial.

The efficacy and safety of high-dose intravenous polyspecific immunoglobulin G (IVIG) as adjunctive therapy in streptococcal toxic shock syndrome (STSS) were evaluated in a multicenter, randomized, double-blind, placebo-controlled trial. The trial was prematurely terminated because of slow patient recruitment, and results were obtained from 21 enrolled patients (10 IVIG recipients and 11 placebo recipients). The primary end point was mortality at 28 days, and a 3.6-fold higher mortality rate was found in the placebo group. A significant decrease in the sepsis-related organ failure assessment score at days 2 (P=.02) and 3 (P=.04) was noted in the IVIG group. Furthermore, a significant increase in plasma neutralizing activity against superantigens expressed by autologous isolates was noted in the IVIG group after treatment (P=.03). Although statistical significance was not reached in the primary end point, the trial provides further support for IVIG as an efficacious adjunctive therapy in STSS.

Adult↗

Rapid diagnosis of active tuberculosis by detecting antibodies from lymphocyte secretions.

In the present study, we investigated the tuberculosis (TB) diagnostic performance of an assay on the basis of detection of TB-specific antibodies from peripheral blood mononuclear cells (PBMCs), to determine whether antibodies in lymphocyte secretions obtained from PBMCs would better reflect active disease than antibodies in serum. PBMCs from patients with and without TB cultured in various concentrations for different times were assessed. Immunoglobulin G (IgG) specific for antigen (bacille Calmette-Guérin [BCG] vaccine and purified protein derivative [PPD]) was measured in lymphocyte secretions. Patients with active TB had higher BCG- or PPD-specific IgG antibody responses than patients without TB or healthy subjects (P=.001). This method can be used as a quick diagnostic aid to facilitate rapid detection of TB cases.

Acute Disease↗

Suppression of leukemia inhibitor factor in lymphoid tissue in primary HIV infection: absence of HIV replication in gp130-positive cells.

BACKGROUND: Leukemia inhibitor factor (LIF), a member of the interleukin-6 cytokine family, has recently been shown to inhibit HIV-1 replication both in vivo and in vitro. OBJECTIVE: LIF and its corresponding receptors gp130 and LIF receptor-alpha (LIFR-alpha) were studied in lymphoid tissue (LT) to reveal potential systemic immunoregulatory effects during the course of HIV-1 infection. METHODS: LIF, gp130, LIFR-alpha and HIV-1 replicating cells were identified at the single cell level by immunohistochemistry and quantified by computerized in situ imaging in tonsil and lymph nodes biopsies (LT) from patients with primary HIV-1 infection (PHI), chronic HIV-1 infection (cHI), long-term non-progressors (LTNP) and HIV-1 seronegative controls. RESULTS: LIF and its receptors, gp130 and LIFR-alpha were significantly (P < 0.005) upregulated in LT from PHI patients as compared with HIV-1 seronegative controls. Expression of LIF in cHI was comparable to LIF levels in HIV-1 seronegative controls whereas LTNP showed significantly reduced LIF expression (P < 0.05). LIF receptors, gp130 and LIFR-alpha were significantly upregulated in cHI (P < 0.005) but downregulated in LTNP (P < 0.05 and P < 0.005, respectively). LIF expressing cells could be demonstrated in LT 2 days after onset of acute retroviral syndrome. LIF expression was evident in CD3, CD4 and CD8 cells. Furthermore, high plasma viral load was associated with high expression of LIF in LT. Finally, no HIV-1 replication could be found in CD4 gp130-positive cells in PHI. CONCLUSIONS: LIF, gp130 and LIFR-alpha showed increased expression in LT from patients with PHI. Furthermore, HIV-1 replication did not occur in cells expressing the LIF signaling receptor, gp130, indicating that LIF may be associated with control of HIV-1 replicating cells in vivo.

Adolescent↗

In interleukin-7-transgenic mice, increasing B lymphopoiesis increases follicular but not marginal zone B cell numbers.

Follicular and marginal zone B cells constitute the vast majority of mature B cells in the adult spleen. The inter-relationships between these two functionally and phenotypically distinct subpopulations of B cells remain unclear. In situations of decreased bone marrow B lymphopoiesis, the proportion of spleen marginal zone B cells increases, but the consequence of increasing B lymphopoiesis on marginal zone B cells has not been investigated. Using interleukin-7-transgenic mice, in which B lymphopoiesis is significantly increased, we show that the number of follicular B cells increased about fivefold but the number of marginal zone B cells decreased. Functional and phenotypic analysis, including in vivo bromodeoxyuridine labeling experiments, showed that marginal zone B cells in transgenic mice were indistinguishable from controls. Mixed radiation bone marrow chimeras showed that marginal zone B cells developed equally well from both normal and transgenic adult bone marrow B cell progenitors. Taken together, these results suggest that interleukin-7 does not influence the lineage choice between follicular and marginal zone B cells and that the number of cells in each compartment is independently regulated.

Animals↗

Persistence of mucosal mast cells and eosinophils in Shigella-infected children.

Cells of the innate immune system and their mediators were studied at the single-cell level in the rectums of pediatric and adult patients with Shigella infection to better understand why children are at higher risk for severe infection. Adult patients had increased infiltration of mucosal mast cells (MMC) at the acute stage (3 to 5 days after the onset of diarrhea) and eosinophils in early convalescence (14 to 16 days after onset). Increased expression of stem cell factor and prostaglandin H synthase-1 (PGHS-1) was associated with increased tryptase-K(i)67-double-positive MMC in the acute stage and increased apoptosis of MMC, which led to a rapid decline in early convalescence. The eosinophils demonstrated increased expression of major basic protein (MBP), eotaxin, and CCR3, as well as increased necrotic death. The neutrophils showed enhanced alpha-defensin and lactoferrin expression in the acute phase. In contrast to adults, the pediatric patients demonstrated delayed accumulation of mast cells and eosinophils, while alpha-defensin expression persisted during convalescence. In contrast, neutrophil counts and lactoferrin expression were reduced in children compared to adults. The results suggest that children with shigellosis have a persistent activation of the innate immune response in the convalescent phase, indicating delayed elimination of Shigella antigens compared to adults.

Adolescent↗

Induction of HIV-1-specific immunity after vaccination with apoptotic HIV-1/murine leukemia virus-infected cells.

Ag-presenting dendritic cells present viral Ags to T cells after uptake of apoptotic bodies derived from virus-infected cells in vitro. However, it is unclear whether apoptotic virus-infected cells are capable of generating immunity in vivo. In this study, we show that inoculation of mice with apoptotic HIV-1/murine leukemia virus (MuLV)-infected cells induces HIV-1-specific immunity. Immunization with apoptotic HIV-1/MuLV-infected syngeneic splenocytes resulted in strong Nef-specific CD8(+) T cell proliferation and p24-induced CD4(+) and CD8(+) T cell proliferation as well as IFN-gamma production. In addition, systemic IgG and IgA as well as mucosa-associated IgA responses were generated. Moreover, mice vaccinated with apoptotic HIV-1/MuLV cells were protected against challenge with live HIV-1/MuLV-infected cells, whereas mice vaccinated with apoptotic noninfected or MuLV-infected splenocytes remained susceptible to HIV-1/MuLV. These data show that i.p. immunization with apoptotic HIV-1-infected cells induces high levels of HIV-1-specific systemic immunity, primes for mucosal immunity, and induces protection against challenge with live HIV-1-infected cells in mice. These findings may have implications for the development of therapeutic and prophylactic HIV-1 vaccines.

AIDS Vaccines↗

Delayed anti-kappa response in kappa-deficient mice after neonatal, oral immunization with kappa-containing IgG.

Antibody responses to kappa (kappa)-light (L) chain are absent in normal (Ckappa+/+) animals because of tolerance due to the abundance of kappa-L chains expressed on more than 95% of all B cells and serum Ig.When heterozygous kappa-sufficient (Ckappa+/-) females are bred with homozygous kappa-deficient (Ckappa-/-) males, half of their offspring will become kappa-deficient but have received kappa-L chain containing maternal Ig, mainly IgG and IgA, through placental and intestinal transmission. The kappa-containing maternal Ig persists for more than 2 months in the circulation of the offspring. Starting from weeks 15 to 20 of age, a spontaneous antibody response towards the maternal kappa-L chains can be recorded. The time of onset, as well as the magnitude of the responses differ among individuals of the same litter. Invariably, once a response has been initiated, it transits into an IgG-type of response, which upon injection with kappa-containing protein shows the features of a secondary type of immune response.

Administration, Oral↗

Oxygen saturation and cognitive performance.

The purpose of the experiments was to investigate how inhalation of 100% oxygen affected cognitive performance. A test battery was developed that was designed to capture different aspects of cognitive processes, i.e., perception, attention, working memory, long-term memory and prospective memory. All tests were verbally based, thus reducing cognitive spatial processes to a minimum. In experiment 1, 48 participants volunteered in a complete factorial within-participant design. Two different conditions for type of gas were used, inhalation of 100% oxygen and inhalation of breathing air (approximately 21% oxygen balanced with nitrogen). The inhalation was performed during the 1 min prior to starting each separate test. The instructions for each test were given during the inhalation period. All participants inhaled oxygen or breathing air through a Swedish military pilot mask. Physiological (heartbeats per minute and blood oxygen saturation level) reactions were recorded continuously throughout the session. Participants also completed a mood-state questionnaire before and after the test battery. The results revealed that cognitive performance were not affected by inhalation. Hence, this experiment does not replicate previous findings that suggest that inhalation of 100% oxygen could increase cognitive performance. Another experiment was performed to control for methodological issues. Experiment 2 revealed exactly the same pattern, i.e., inhalation of oxygen did not affect cognitive functioning.

Administration, Inhalation↗

Low levels of perforin expression in CD8+ T lymphocyte granules in lymphoid tissue during acute human immunodeficiency virus type 1 infection.

Human immunodeficiency virus (HIV)-specific cytotoxic T lymphocyte (CTL) responses are detectable shortly after the acute phase of HIV infection, but they cannot control viral replication and prevent development of chronic immune suppression. This article describes a defect in the coexpression of perforin in granzyme A-positive CD8(+) T cells in lymphoid tissue from patients with acute HIV infection and a reduction in the perforin-dependent nuclear translocation of granzyme A. Furthermore, intracellular levels of HIV DNA and RNA found in lymphoid tissue were higher (10-100 times) than those found in blood, and blood samples showed more-coordinated cellular perforin/granzyme A expression. This suggests that mechanisms inhibiting CTL-mediated cytotoxicity are operative in lymphoid tissue early in the course of HIV infection.

Acquired Immunodeficiency Syndrome↗

Accumulation of DC-SIGN+CD40+ dendritic cells with reduced CD80 and CD86 expression in lymphoid tissue during acute HIV-1 infection.

BACKGROUND: Dendritic cells (DC) are target cells for HIV-1 and play a key role in antigen presentation and activation of T cells. OBJECTIVE: To characterize interdigitating DC in lymphoid tissue (LT) with regard to maturation, expression of cytokines and co-stimulatory molecules in HIV-1-positive patients. METHODS: DC were characterized by immunohistochemistry and in situ imaging in LT from patients with acute HIV-1 infection (aHI), antiretroviral treated patients, long-term non-progressors/slow progressors with HIV-1 infection (LTNP/SLP), patients with AIDS, HIV-1-negative controls and patients with acute Epstein-Barr virus (EBV) infection. RESULTS: A significant increase of interdigitating DC expressing CD1a, S-100b, CD83 and DC-SIGN was found in LT from patients with aHI (P < 0.02). The co-stimulatory molecules CD80 and CD86 were, however, only partially upregulated and the complete parafollicular network found in acute EBV infection was not generated, despite increased expression of interleukins 1alpha, 1beta, 12; interleukin 1alpha receptor antagonist; interferon alpha; and CD40 expression. LTNP/SLP and treated aviremic subjects had increased frequency of interdigitating DC, albeit lower than in aHI, and low expression of CD80 and CD86. In contrast, patients with AIDS had fewer DC and reduced cytokine expression in LT. CONCLUSIONS: In the early phase of HIV-1 infection, there was a migration of DC to LT comparable to that found in acute EBV infection. The infiltration of DC in LT in acute EBV infection was accompanied by upregulation of CD80 and CD86 expression, which did not occur in aHI. This co-stimulatory defect in aHI may have an impact on the development of HIV-1-specific T cell immunity.

Acute Disease↗

Parallel decline of CD8+/CD38++ T cells and viraemia in response to quadruple highly active antiretroviral therapy in primary HIV infection.

OBJECTIVES: To monitor changes in the numbers of CD8 lymphocytes expressing the activated CD38++ phenotype in peripheral blood samples from patients with primary HIV infection (PHI) treated with highly active antiretroviral therapy (HAART). METHODS: Zidovudine, lamivudine, abacavir and amprenavir were initiated during PHI as part of the Quest study. Absolute numbers of CD8+/CD38++ T cells were determined using three-colour flow cytometry, and plasma viral load (VL) was measured using the Roche Amplicor method. RESULTS: The median, pre-therapy CD8+/CD38++ T cell count was 461/mm(3)(interquartile range 216, 974) in 131 patients compared with normal control values of less than 20 cells/mm(3). Levels fell markedly in parallel with VL within the first 2 weeks of HAART initiation, to a median of 47 cells/mm(3) at 28 weeks (median 436 cell decline; P < 0.001). At that time, 80% of patients had a VL less than 50 copies/ml, and 16.3% of all patients had less than 20 CD8+/CD38++ T cells/mm(3). A continued decrease in CD8+/CD38++ T cell count occurred in 67.2% of patients whose VL was maintained below 50 copies/ml (median change from first to last value -18 cells/mm(3); P < 0.001). CONCLUSION: After the initiation of HAART in PHI, CD8+/CD38++ lymphocytes declined rapidly in parallel with VL, and allowed for a normalization of CD8+/CD38++ T cell numbers in a subset of patients at week 28. Cell numbers continued to decline in patients who maintained VL below 50 copies/ml, indicating that the CD8+/CD38++ T cell count may represent a marker of residual viral replication when VL falls below detectable levels after HAART intervention.

Adult↗

Constitutive and inflammatory induction of alpha and beta chemokines in human first trimester forebrain astrocytes and neurons.

Chemokine effects on leukocyte infiltration into the central nervous system (CNS) are key events in the inflammatory processes of neuroimmunologic and neuroinfectious diseases. Because, chemokines may play important roles in proliferation and differentiation of brain cells and in the initiation and progression of CNS inflammatory disorders, we analyzed constitutive and inflammatory-induced expression of alpha and beta chemokines in human first trimester forebrain cells. Constitutive induction of IL-8, MIP-1alpha, MIP-1beta, MCP-1 and regulated on activation, normal T-cell expressed, and secreted (Rantes) was detected in cryostat sections of embryonic forebrains in an age-dependent manner. Dissociated cell cultures were studied for spontaneous chemokine induction and after stimulation with the trypanosome lymphocyte triggering factor (TLTF), a novel trypanokine secreted by African trypanosomes that triggers a complex of immune responses. LPS and variant surface glycoprotein (VSG) were used as controls. In cultures, unstimulated cells expressed minimal chemokine levels except for Rantes. In response to TLTF and LPS, but not VSG, all chemokines were highly induced at the mRNA and protein levels in a dose- and age-dependent manner. Combined assays (in situ hybridization and immunohistochemistry) revealed that astrocytes and neurons are major sources for chemokines. These results illustrate the ability of resident brain cells to constitutively express chemokine genes, which may suggest an important role for chemokines during brain development. Furthermore, TLTF-induced chemokine expression in astrocytes and neurons indicate the capacity of TLTF to provoke neuroinflammation in the brain, which may have important therapeutic implications for the neurological manifestations of African trypanosomiasis.

Astrocytes↗

Mobius sequence--a Swedish multidiscipline study.

Mobius sequence/syndrome is a rare disorder characterized by congenital palsy of the 6th and 7th cranial nerves. Other cranial nerves may be affected, skeletal and orofacial anomalies and mental retardation occur. The aims were to determine the frequency of associated clinical characteristics and to identify any pregnancy or environmental factors in patients with Mobius sequence. A prospective study of 25 Swedes with apparent involvement of the 6th and 7th cranial nerves was performed and 25 patients, 1 month to 55 years old, were examined. Obvious associated systemic anomalies observed included: limb malformations (10), Poland anomaly (2), hypodontia (7), microglossia (6), cleft palate (4), hearing impairment (5) and external ear malformation (1). Pronounced functional abnormalities were observed involving facial expression (16), speech (13), eating and swallowing (12) and difficulty in sucking in infancy (11). Six patients had an autistic syndrome, one an autistic-like condition, and mental retardation was found in all these patients. No common aetiological cause was found but their mothers' pregnancy histories revealed a history of benzodiazepines (1), bleeding during pregnancy (8), spontaneous abortion (7) and chorion villus sampling in the second month of pregnancy (1). In conclusion, many patients had multiple problems with eating and communication resulting from facial palsy, cleft palate and tongue anomalies. Autism and mental retardation was diagnosed in one-third of the patients. Awareness of the wide spectrum of manifestations in Mobius sequence will assist in identification of the associated malformations and functional problems that are often seen and result in better care of the children.

Abducens Nerve Diseases↗

Apoptosis in acute shigellosis is associated with increased production of Fas/Fas ligand, perforin, caspase-1, and caspase-3 but reduced production of Bcl-2 and interleukin-2.

Shigella dysenteriae type 1-induced apoptotic cell death in rectal tissues from patients infected with Shigella dysenteriae type 1 was studied by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique and annexin V staining. Expression of proteins and cytokines participating in the apoptotic process (caspase-1, caspase-3, Fas [CD95], Fas ligand [Fas-L], perforin, granzyme A, Bax, WAF-1, Bcl-2, interleukin-2 [IL-2], IL-18, and granulocyte-macrophage colony-stimulating factor) in tissue in the acute and convalescent stages of dysentery was quantified at the single-cell level by in situ immunostaining. Apoptotic cell death in the lamina propria was markedly up-regulated at the acute stage (P < 0.05), where an increased number of necrotic cells were also seen. Phenotypic analysis of apoptotic cells revealed that 43% of T cells (CD3), 10% of granulocytes (CD15), and 5% of macrophages (CD56) underwent apoptosis. Increased activity of caspase-1 persisted in the rectum up to 1 month after onset. More-extensive expression of Fas, Fas-L, perforin, caspase-3, and IL-18, but not IL-2, at the acute stage than at the convalescent stage was observed. Increased expression of caspase-3 and IL-18 in tissues with severe inflammation compared to expression in those with mild inflammation was evident, implying a possible role in the perpetuation of inflammation. Significantly reduced cell death during convalescence was associated with a significant up-regulation of Bcl-2, Bax, and WAF-1 expression in the rectum compared to that in the acute phase of infection. Thus, induction of apoptosis at the local site in the early phase of S. dysenteriae type 1 infection was associated with a significant up-regulation of Fas/Fas-L and perforin and granzyme A expression and a down-regulation of Bcl-2 and IL-2, which promote cell survival.

Acute Disease↗

Endogenous inhibitors of HIV: potent anti-HIV activity of leukemia inhibitory factor.

The correlates of protective immunity in HIV-1 infection include the endogenous production of compounds with anti-HIV-1 activity. These compounds can be produced independently of specific humoral or cellular immune responses. A model of compartmental inhibition of HIV-1 infection is the placenta, an organ that prevents transmission of HIV-1 to the fetus in the majority of HIV-1 pregnancies. Studies of this organ elucidated new compounds and mechanisms for prevention and treatment of HIV including the potent inhibitor of HIV-1, leukemia inhibitory factor (LIF). Besides coordinating the humoral and cellular immune responses, cytokines such as IFN-gamma exhibit intrinsic antiviral activity that represents the first line of defense against pathogens prior to the development of a specific immune response. The study of antiviral factors is particularly important in HIV/AIDS because of the direct destruction of the immune system by HIV-1. In this report, we focus on the identification and mechanism of endogenously produced anti-HIV factors and the overall function of these factors in the prevention and treatment of HIV/AIDS.

Animals↗

An Overview of Epstein-Barr Virus: from Discovery to Future Directions for Treatment and Prevention.

Discovered in 1964 by Epstein and Barr, the Epstein-Barr virus (EBV) is widespread in all areas of the world, infecting over 95% of the adult population and earning it the informal name, 'Every Body's Virus'. It was shown to be the causal agent of infectious mononucleosis (IM) in 1968, and many reports followed linking EBV to several other clinical syndromes. In 1970, the virus was shown to be able to immortalize B lymphocytes, which are one of its target cells. This oncogenic potential underlies the role of EBV in Burkitt's lymphoma, post-transplant lymphoproliferative disorders and lymphoma in HIV-infected patients. In addition, EBV can infect epithelial cells in the nasopharynx and is a co-factor for development of nasopharyngeal carcinoma. There is no treatment available for IM to date; however, virus-associated complications may be treated with various modes of immune modulation. Currently, radiotherapy and chemotherapy remain the main treatments for EBV-associated malignancies. Recent evidence has suggested that adoptive therapy through infusions of human leukocyte-associated antigen-matched EBV cytotoxic T cells may form a novel strategy for both prophylaxis and treatment of EBV-induced lymphoproliferative disorders. Additionally, a vaccine based on immunization with a structural antigen, gp350, is under evaluation.

Journal Article↗

Determination of cytomegalovirus DNA load for monitoring of cytomegalovirus disease and antiviral treatment in solid organ transplant patients, comparing limiting-dilution PCR and hybrid capture assay with cytomegalovirus isolation.

OBJECTIVE: To improve the identification of patients at risk of developing cytomegalovirus (CMV) disease. MATERIALS AND METHODS: In a prospective study of 50 kidney or liver transplant patients who developed fever, 133 EDTA blood samples were analyzed, using two tests to measure CMV DNA: a 10-fold limiting dilution of an extract of 2 million leukocytes for CMV PCR, and a CMV hybrid capture assay. Both tests were compared with virus isolation, using an equivalent amount of leukocytes as a base for all three tests. RESULTS: The limiting-dilution CMV PCR and the hybrid capture assay presented relatively similar changes of sensitivity and specificity at different CMV DNA concentrations. The kinetics of the positive and negative predictive values were also comparable. A higher CMV DNA load corresponded to an increased risk of developing CMV disease. Furthermore, an increase in the endpoint dilution of a positive CMV PCR also corresponded to more severe disease. After antiviral treatment, the CMV PCR decreased by at least 100-fold (2 log10) in 10 cases and by 10-fold (1 log10) in five cases. Thus, there was a decrease in 15 of 18 (83%) patients. Similarly, with the hybrid capture assay, the amount of CMV DNA decreased about 100-fold in five patients and decreased by about 0.5 genome equivalents in five cases, i.e. in 10 of 12 (83%) patients. CONCLUSION: Both methods proved clinically useful for detecting patients at risk of developing CMV disease and for monitoring antiviral treatment in solid organ transplant patients.

Journal Article↗