Cells from a human lymphoblastoid cell line (Raji), with B-cell characteristics, and having receptors for human IgG Fc, C3b, and C3d, were used in an immunofluorescence test as in vitro detectors of immune complexes in animal and human sera. By this test, as little as 200-300 ng aggregated human gamma globulin or immune complexes per ml serum could be detected. The receptors for IgG Fc on the Raji cells were shown to be inefficient in detecting aggregated human gamma globulin and binding of aggregates to these receptors was inhibited by physiologic concentrations of 7S human IgG. Enhancement of aggregated human gamma globulin binding and binding of immune complexes formed in vitro to Raji cells was observed when the receptors for complement on these cells were used. By using the receptors for complement on Raji cells, circulating immune complexes were detected in rabbits with acute serum sickness, in mice with acute lymphocytic choriomeningitis virus infection, and in humans with immune complex ...

What is the difference between Latent and Persistent Viral Infection? Clinical features are present only during persistent stage of viral infection. In latent..

Co-Author, The Evidence of Things Not Seen: Non-Matches as Evidence of Innocence, 98 Iowa L. Rev. 577 (2013). Co-Author, Toll-like receptor 7 is required for effective adaptive immune responses that prevent persistent virus infection, Cell Host Microbe., 2012 Jun.. Angelosanto JM, Blackburn SD, Crawford A, Wherry EJ, Progressive loss of memory T cell potential and commitment to exhaustion during chronic viral infection. J Virol., 2012 Aug.. Crawford A, Angelosanto JM, Nadwodny KL, Blackburn SD, Wherry EJ, A role for the chemokine RANTES in regulating CD8 T cell responses during chronic viral infection. PLoS Pathog., 2011 Jul.. Blackburn SD, et al., Tissue-specific differences in PD-1 and PD-L1 expression during chronic viral infection: implications for CD8 T-cell exhaustion. J Virol., 2010 Feb.. Shin H, Blackburn SD, et al., A role for the transcriptional repressor Blimp-1 in CD8(+) T cell exhaustion during chronic viral infection. Immunity, 2009 Aug.. Blackburn SD, et al. Co-regulation of CD8 T ...

Lymphocytic choriomeningitis (LCM) is a rodent-borne viral infectious disease that presents as aseptic meningitis, encephalitis or meningoencephalitis. Its causative agent is the lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae. The name was coined by Charles Armstrong in 1934. The Gale Encyclopedia of Medicine defines lymphocytic choriomeningitis (LCM) as a viral infection of the membranes surrounding the brain and spinal cord and of the cerebrospinal fluid. The name is based on the tendency of an individual to have abnormally high levels of lymphocytes during infection. Choriomeningitis is cerebral meningitis in which there is marked cellular infiltration of the meninges, often with a lymphocytic infiltration of the choroid plexuses. There are several strains of LCM virus, among which the most widely used are LCMV Armstrong and LCMV Clone 13. Armstrong is the original virus strain which was isolated from the brain by Charles Armstrong in 1934. It triggers a ...

TY - JOUR. T1 - Effect of Chronic Viral Infection on Epitope Selection, Cytokine Production, and Surface Phenotype of CD8 T Cells and the Role of IFN-γ Receptor in Immune Regulation. AU - Tewari, Kavita. AU - Sacha, Jonah. AU - Gao, Xiaoyan. AU - Suresh, M.. PY - 2004/2/1. Y1 - 2004/2/1. N2 - Regulation of CD8 T cell responses in chronic viral infections is not well understood. In this study, we have compared the CD8 T cell responses to immunodominant and subdominant epitopes during an acute and a chronic lymphocytic choriomeningitis virus (LCMV) infection in mice. The epitope hierarchy of the primary CD8 T cell response was similar in acute and chronic LCMV infections. However, strikingly, the epitope hierarchy of the primary CD8 T cell response was conserved in the T cell memory only in an acute but not in a chronic LCMV infection. Interestingly, in an acute infection, increasing the viral dose caused significant changes in the epitope hierarchy of the LCMV-specific memory CD8 T cell pool, ...

Summary As shown previously, after inoculation into the footpad of a mouse the lymphocytic choriomeningitis (LMC) virus multiplies locally. Beginning on day 6 or 7 after infection, the foot undergoes a delayed-type hypersensitivity (DTH) reaction which consists of two distinct phases that are mediated by CD8+ cells and CD4+ cells, respectively, and at about the same time the virus is eliminated. In general, for terminating infection of the mouse with LCM virus the CD8+ cytotoxic/suppressive T lymphocyte (CTL) is essential; we have now determined the cells that mediate control of the virus in a tissue undergoing a specific DTH reaction. Depletion, in infected mice, of all T lymphocytes by treatment with anti-Thy-1 monoclonal antibody prevented virus elimination from the foot, and the same was true when the CD8+ CTLs were removed. Depletion of the CD4+ helper/suppressor subset only marginally impaired the ability of the mice to rid themselves of the virus. The conclusion that here too the principal

Isolates of lymphocytic choriomeningitis virus (LCMV) that elicit a cytotoxic T-lymphocyte response (CTL+) have been compared with isolates that suppress the CTL response (CTL-) in an effort to map this phenotype. A single amino acid change in the glycoprotein of the LCMV Armstrong (ARM) strain is consistently associated with the CTL- trait and the ability of the virus to persist (P+). The CTL+ P- parental strain spontaneously gives rise to CTL- P+ variants within lymphoid tissues of mice persistently infected from birth. To map the structural basis of the phenotype, the complete RNA sequence of LCMV ARM 53b (CTL+) was compared with that of its variant ARM clone 13 (CTL-). Differences in 5 of 10,600 nucleotides were found. Three changes are noted in the large L RNA segment, and two are noted in the small S RNA segment. Only two of the changes distinguishing CTL+ from CTL- isolates affect amino acid coding: lysine to glutamine at amino acid 1079 of the polymerase protein, and phenylalanine to ...

Lymphocytic choriomeningitis virus (LCMV) is a single-stranded RNA virus that belongs to the family Arenaviridae (so named because of its appearance on electron microscopy, which resembles grains of sand). Other members of this family include Lassa virus and the Tacaribe group.

THE interaction of lymphocytic choriomeningitis (LCM) virus with mouse tissues has been discussed recently1-5. The fulminating disease, which occurs in adult mice after intracerebral inoculation with LCM virus, can be ameliorated by several treatments known to impair the immune response of the host, such as X-rays6, amethopterin7, thymectomy8 and anti-lymphocyte serum9. The pathology of the disease10 supports the current view that an immune reaction by the host against the virus or a virus product, located in or on infected cells, plays an essential part in its pathogenesis. A similar mechanism may be important in the chronic autoimmune-like disease in virus carrier mice2,5. Further elucidation of this disease mechanism depends on understanding the nature of the immune response and its target. A question of considerable interest is what the consequences might be for virus infected cells in the event of an immune response against the virus or a virus product. Here we report preliminary experiments

Goldsmith, Cynthia S.; Ksiazek, Thomas G.; Rollin, Pierre E.; Comer, James A.; Nicholson, William L.; Peret, Teresa C.T.; Erdman, Dean D.; Bellini, William J.; Harcourt, Brian H.; Rota, Paul A.; Bhatnagar, Julu; Bowen, Michael D.; Erickson, Bobbie R.; McMullan, Laura K.; Nichol, Stuart T.; Shieh, Wun-Ju; Paddock, Christopher D.; Zaki, Sherif R ...

We determined the prevalence of infection with lymphocytic choriomeningitis virus (LCMV) among small mammals in northern Italy and analyzed long-term dynamics of LCMV in a rodent population in the province of Trento. LCMV is circulating among the most widespread and common wild rodent species in this area (Apodemus flavicollis, Myodes glareolus, and Microtus arvalis); overall prevalence is 6.8%. During 2000-2006, intensive monitoring of LCMV in a population of yellow-necked mice (A. flavicollis) showed a positive correlation between prevalence of infection and rodent density. At the individual level, weight and sex appeared to correlate with antibody prevalence, which suggests that horizontal transmission of LCMV occurs principally among heavier, older males and occurs during fighting. Isolation and genetic characterization of this virus will be the crucial next steps for a better understanding of its ecology.

Persistent infection of C3H/St mice with certain strains of lymphocytic choriomeningitis virus (LCMV) causes a growth hormone (GH) deficiency syndrome (GHDS) manifested as growth retardation and hypoglycemia. Infected mice show high levels of viral replication in the GH-producing cells in the anterior pituitary leading to decreased synthesis of GH mRNA and protein despite the absence of detectable virus-induced cell structural damage. Virus clones isolated from the GHDS-negative LCMV WE strain can cause the disease, while others cannot. The genetic basis of this phenotypic difference is a nucleotide substitution resulting in a single amino acid difference in the viral glycoprotein. Reassortant studies indicate that the single amino acid substitution (Ser-153 to Phe) is sufficient to allow infection of the GH-producing cells and cause GHDS. These results show that a single change in the genome can affect viral pathogenicity by altering the tropism of the virus.

In Vivo Selection of a Lymphocytic Choriomeningitis Virus Variant That Affects Recognition of the GP33-43 Epitope by H-2Db but Not H-2Kb ...

Lymphocytic choriomeningitis virus RNA-directed RNA polymerase L (L) datasheet and description hight quality product and Backed by our Guarantee

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(a) Schematic view of acute and chronic LCMV infections including virus and cytotoxic T lymphocyte (CTL) dynamics. (b) Representation of the CTL-induced immunop

Lymphocytic choriomeningitis: Lymphocytic choriomeningitis, inflammation of the meninges (membranes covering the central nervous system) and choroid plexus (an area of the brain that regulates the

Three clusters of organ transplant-associated lymphocytic choriomeningitis virus (LCMV) transmissions have been identified in the United States; 9 of 10 recipients died. In February 2011, we identified a fourth cluster of organ transplant-associated LCMV infections. Diabetic ketoacidosis developed in the organ donor in December 2010; she died with generalized brain edema after a short hospitalization. Both kidneys, liver, and lung were transplanted to 4 recipients; in all 4, severe posttransplant illness developed; 2 recipients died. Through multiple diagnostic methods, we identified LCMV infection in all persons, including in at least 1 sample from the donor and 4 recipients by reverse transcription PCR, and sequences of a 396-bp fragment of the large segment of the virus from all 5 persons were identical. In this cluster, all recipients developed severe illness, but 2 survived. LCMV infection should be considered as a possible cause of severe posttransplant illness ...

The main reservoir of LCMV, which belongs to the arenaviruses, is the house mouse. Cells infected with LCMV express antigens and are recognised by cytotoxic T lymphocytes. This lymphocyte activity also makes the blood-brain barrier permeable resulting in meninges and neurons being damaged. Infection of adult mice leads to choriomeningitis. In contrast, an intrauterine or neonatal infection generally causes an asymptomatic chronic carrier state in mice, with such animals forming immune complexes in the course of their lifetime that lead to glomerulonephritis. In guinea pigs and hamsters, LCMV infections often progress subclinically, however, conjunctivitis, blepharitis, respiratory symptoms, tremor, seizures and paralysis have been described. LCMV is transmitted diaplacentally and with all secretions and excretions. In humans, LCMV rarely leads to choriomeningitis; the infection is usually asymptomatic or shows mild, flu-like symptoms. An infection in the second part of pregnancy can cause severe ...

To establish if a correlation exists between the expansion of GP33-specific cells observed by flow cytometry and GP33-specific cytotoxicity, direct CTL assays were carried out using spleen cells from the mice described above. CTL activity mediated by antigen-specific CD8+ cells is usually difficult to measure at day 3 after infection since LCMV induces, at this early time point, strong NK cell activity that lyses both antigen-pulsed and unpulsed target cells. To circumvent this problem, direct CTL assays were carried out by adding a twofold excess of unlabeled NK-sensitive target cells (YAC-1 cells) to assay wells as cold-target competitors. Inclusion of cold YAC-1 cells abrogated lysis of chromium-labeled MC57 target cells by NK cells from the spleens of mice that had been injected 48 h previously with poly-IC (data not shown). No inhibition of antigen-specific CTLs was observed when YAC-1 cells were included as cold-target competitors in a direct CTL assay using spleen cells from mice that had ...

To date, everything written about Armstongs life and flights has been written from the outside looking in; Barbree is the only person whom Neil Armstrong trusted to share close personal details about his inspiring life story.. Working from his years of notes, and with the full cooperation of the Armstrong family, Barbree has written the definitive biography of Americas most famous astronaut and one of our greatest modern heroes. Much has already been written about Armstrong and the major players who helped him fly to the moon, but he wanted this book to emphasize his two passions-family and flight. Barbree and Armstrong discussed everything, from his two marriages and the death of his baby daughter, to his love of flying, the war years and of course, his time in space. The book, timed to coincide with the 45th anniversary of the Apollo 11 launch and full of never-before-seen photos, includes many personal details that have never before been written, such as what Armstrong really felt when he ...

Katrina Armstrong, MD, MSCE, a world-renowned investigator in the areas of medical decision-making, quality of care and cancer prevention and outcomes, has been selected as the MGHs next physician-in-chief of the MGH Department of Medicine. Armstrong will succeed internationally regarded physician-scientist Dennis Ausiello, MD, who has led the department since 1996.. Armstrong, who currently serves as chief of the Division of General Medicine and professor of Medicine and Obstetrics and Gynecology at the Perelman School of Medicine at the University of Pennsylvania, will start in the new position April 15. We are at a time of unparalleled opportunity to advance science, education and clinical care to benefit our patients and our communities, says Armstrong. MGH is an extraordinary institution with a long tradition of leadership in internal medicine, and I am honored to become part of that tradition.. Armstrong is a graduate of Yale University and Johns Hopkins University School of Medicine ...

Armstrong was promoted to the rank of Lieutenant with seniority of 13 November, 1892.[1] He married Ethel M. Heath on 23 February, 1893 at Kensington.[2] He was appointed in command of the destroyer Lynx on 3 August, 1897.[3] On 15 October, 1897, Armstrong was tried at a Court Martial for negligently stranding Lynx while following Thrasher in dense fog off the Cornish coast. He was acquitted.[4][5][6][7] In September, 1902, Armstrong was credited with the cleaver capture of a pair of pirate dhows at Bussorah.[8] He was promoted to the rank of Commander dated 1 January, 1903.[9] After commanding Lively in the 1903 manoeuvres, Armstrong undertook a war course and a senior officers gunnery course and was then appointed to the second class protected cruiser Challenger on 3 May, 1904. Upon paying her off on 20 July, 1906, he was appointed to Hyacinth, to assume command, temporarily for one month from 20 December, 1906.[10] Armstrong was promoted to the rank of Captain on 31 December, 1908.[11] On ...

Armstrong was promoted to the rank of Lieutenant with seniority of 13 November, 1892.[1] He married Ethel M. Heath on 23 February, 1893 at Kensington.[2] He was appointed in command of the destroyer Lynx on 3 August, 1897.[3] On 15 October, 1897, Armstrong was tried at a Court Martial for negligently stranding Lynx and was acquitted.[4] In September, 1902, Armstrong was credited with the cleaver capture of a pair of pirate dhows at Bussorah.[5] He was promoted to the rank of Commander dated 1 January, 1903.[6] After commanding Lively in the 1903 manoeuvres, Armstrong undertook a war course and a senior officers gunnery course and was then appointed to the second class protected cruiser Challenger on 3 May, 1904. Upon paying her off on 20 July, 1906, he was appointed to Hyacinth, to assume command, temporarily for one month from 20 December, 1906.[7] Armstrong was promoted to the rank of Captain on 31 December, 1908.[8] On 12 February, 1910, he was appointed in command of the repair ship ...

In Fröhjahr 1998 kehr Lance Armstrong in den Radsport torüch. Intüschen bi dat amerikaansch Team US Postal Service ünner Verdrag, weer de Neeanfang tonächst nich spoodriek. Eerst in tweeten Anloop in Harvst vun dat glieker Johr kunn sück Lance Armstrong weer in Szene setten un keem bi de Vuelta a España sensationell den veerten Platz, de bit dorhen best Platzeeren vun den eenstigen Klassikerspezialisten bi en grooten Rundfohrt. 1999 wunn Armstrong eerstmals de Tour de France as ok veer eenzelt Deelstrecken. Up de Bargetappen un besünners in Tietfohren hett he sien Vörsprung immer wieder utbaut. Armstrong sien Sieg wurr weltwiet as dat „Comeback des Jahrhunderts fiert. Armstrong kunn sien Sieg bi de Tour in den Folgejohren 2000 bit 2005 wedderhalen. He hett sien gesamte Saisonplanung nipp un nau up de dree Week düernd Rundfohrt in Frankriek utricht, wat hüm woll de Kritik vun Expertensiet inbrocht hett, aber spoodriek weer. Neben bzw. in Rahmen vun sien Tour-Vörbereiten kunn ...

tags: hamster, PetSmart, lawsuit, lymphocytic choriomeningitis virus, LCMV, zoonosis Portrait of a murderer: A Siberian dwarf hamster, Phodopus sungorus. Orphaned image. I just learned that a lawsuit was recently filed in Massachusetts Superior Court on behalf of a man who died one month after receiving a transplanted liver that was later determined to be infected…. ...

Jan. 2001-present SCIENTIFIC PUBLICATIONS: 1 Beck,M.L., S.H. Butch, W.R. Armstrong, and H.A. Oberman. An Auto-antibody with U- Specificity in a Patient with Myasthenia Gravis. Transfusion, 12:280:1972. 2. VanKirk,I.E., A.B. Simon, and W.R. Armstrong. Candida Myocarditis Causing Complete Heart Block. JAMA 25, Feb74, p.931-33. 3. Amistrong,W.R. and E.W. Catalano. The PAS Stain in Acute Leukemia - Increased Sensitivity with Diastase. Am.J.Clin.Path. 72:652, 1979. 4. Godder,K, Pati,AR, Abhyankar,SH, Lamb,LS, Armstrong,W and Henslee-Downey, J: De-novo Chronic Graft versus Host Disease Presenting as Hemolytic Anemia Following Partially Mismatched Related Donor Bone Marrow Transplant. Bone Marrow Transplant 19:813-817, 1997. 5. Thurer,Robert L, Luban,N., AuBuchonjP, et al: Universal WBC Reduction. Letters to the Editor, Transfusion 40:751-2, June 2000. PRESENTATIONS: 1 Armstrong,W.R. Fibrous Histiocytic Neoplasms. Department of Postgraduate Medicine, University of Michigan, 4/73. M.R. Abell, MD, ...

AUSTIN, Texas (AP) - Lance Armstrong is facing more doping allegations just a few months after he thought he had finally put them to rest. Although federal investigators in February closed a two-year investigation without bringing criminal charges, the U.S. Anti-Doping Agency has filed new doping charges that could strip the seven-time Tour de France winner of his victories in cyclings premier race. Armstrong insists he is innocent. I have never doped, and, unlike many of my accusers, I have competed as an endurance athlete for 25 years with no spike in performance, passed more than 500 drug tests and never failed one, Armstrong said in a statement. Any fair consideration of these allegations has and will continue to vindicate me. The move by USADA immediately bans him from competing in triathlons, which he turned to after he retired from cycling last year. Armstrong has been dogged by doping allegations since his first Tour victory in 1999, but had hoped his fight to be viewed as a clean

Video articles in JoVE about t lymphocytes cytotoxic include A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses, A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl, Radial Mobility and Cytotoxic Function of Retroviral Replicating Vector Transduced, Non-adherent Alloresponsive T Lymphocytes, Murine Lymphocyte Labeling by 64Cu-Antibody Receptor Targeting for In Vivo Cell Trafficking by PET/CT, Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice, Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining, Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development, A Flow Cytometry-Based Cytotoxicity Assay for the Assessment

TY - JOUR. T1 - 4-1BB signaling synergizes with programmed death ligand 1 blockade to augment CD8 T cell responses during chronic viral infection. AU - Vezys, Vaiva. AU - Penaloza-Macmaster, Pablo. AU - Barber, Daniel L.. AU - Ha, Sang Jun. AU - Konieczny, Bogumila. AU - Freeman, Gordon J.. AU - Mittler, Robert S.. AU - Ahmed, Rafi. PY - 2011/8/15. Y1 - 2011/8/15. N2 - Previous studies have identified the inhibitory role that the programmed death 1 (PD-1) pathway plays during chronic infection. Blockade of this pathway results in rescue of viral-specific CD8 T cells, as well as reduction of viral loads in mice chronically infected with lymphocytic choriomeningitis virus (LCMV). We tested the effect of combining PD ligand 1 (PD-L1) blockade with an agonistic regimen that induces 4-1BB costimulation during chronic LCMV infection. There is a boosting effect in the rescue of LCMV-specific CD8 T cell responses after dual treatment with PD-L1 blockade and 4-1BB agonistic Abs when the amount and timing ...

Infections induce complex host responses linked to antiviral defense, inflammation, and tissue damage and repair. We hypothesized that the liver, as a central metabolic hub, may orchestrate systemic metabolic changes during infection. We infected mice with chronic lymphocytic choriomeningitis virus (LCMV), performed RNA sequencing and proteomics of liver tissue, and integrated these data with serum metabolomics at different infection phases. Widespread reprogramming of liver metabolism occurred early after infection, correlating with type I interferon (IFN-I) responses. Viral infection induced metabolic alterations of the liver that depended on the interferon alpha/beta receptor (IFNAR1). Hepatocyte-intrinsic IFNAR1 repressed the transcription of metabolic genes, including Otc and Ass1, which encode urea cycle enzymes. This led to decreased arginine and increased ornithine concentrations in the circulation, resulting in suppressed virus-specific CD8+ T cell responses and ameliorated liver ...

Lymphocytic Choriomeningitis (LCM) Lymphocytic choriomeningitis, or LCM, is a rodent-borne viral infectious disease caused by lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae that was initially isolated in 1933. The primary host of LCMV is the common house mouse, Mus musculus. Infection in house mouse populations may vary by geographic location, though it is estimated that 5% of house mice throughout the United States carry LCMV and are able to transmit virus for the duration of their lives without showing any sign of illness. Other types of rodents, such as hamsters, are not the natural reservoirs but can become infected with LCMV from wild mice at the breeder, in the pet store, or home environment. Humans are more likely to contract LCMV from house mice, but infections from pet rodents have also been reported.. LCMV infections have been reported in Europe, the Americas, Australia, and Japan, and may occur wherever infected rodent hosts of the virus are found. The ...

Infections induce complex host responses linked to antiviral defense, inflammation, and tissue damage and repair. We hypothesized that the liver, as a central metabolic hub, may orchestrate systemic metabolic changes during infection. We infected mice with chronic lymphocytic choriomeningitis virus …

Summary A quantal microassay for the titration of LCM virus strains is described. It is based on the detection of virus-specific complement-fixing antigen in the medium of infected L cell microcultures.

Adoptive immunization of syngeneic, immunosuppressed recipients infected with lymphocytic choriomeningitis (LCM) virus causes fatal neurologic disease within 2 to 4 days of cell transfer, providing that donors are sampled when the in vitro 51Cr release assay shows maximal specific activity of sensitized thymus-derived lymphocytes (T cells). Prior treatment of immune spleen cells with AKR anti-θ ascitic fluid and complement causes total abrogation of this in vivo activity. Fatal neurologic disease is induced only when donor and recipient share at least one set of H-2 antigenic specificities. Parent → F1 and F1 → parent combinations are as effective as syngeneic systems, but mice given allogeneic immune cells survive as long as controls. Differences at the M-locus in H-2 compatible mice do not inhibit effector activity. Homing of transferred lymphocytes to spleen is similar in syngeneic or allogeneic recipients, but only syngeneic immune cells cross the blood-cerebrospinal fluid (CSF) barrier ...

In a mouse colony in which lymphocytic choriomeningitis is endemic infection takes place either in utero or shortly after birth. Virus is discharged from infected mice with the nasal secretions and urine. In some mice the infection lasts for several months, and such carriers can transmit the disease to healthy mice by contact. The portal of entry appears to be the nasal mucosa rather than the gastrointestinal tract. Mice infected by contact show no definite symptoms while those infected in utero often do. The disease has persisted in the colony for at least 15 months without change in its character. Mouse stocks differ in their susceptibility to contact infection and the findings given in the paper could be reproduced only with a very susceptible stock. Wild mice (Mus musculus) can be infected by contact, although less easily than our white mice.. The source of the infection in the colony has not been determined. The fact that the serum of the caretaker neutralizes the virus indicates that he ...

We use simple mathematical models to examine the dynamics of primary and secondary cytotoxic T-lymphocyte (CTL) responses to viral infections. In particular, we are interested in conditions required to resolve the infection and to protect the host upon secondary challenge. While protection against reinfection is only effective in a restricted set of circumstances, we find that resolution of the primary infection requires persistence of CTL precursors (CTLp), as well as a fast rate of activation of the CTLp. Since these are commonly the defining characteristics of CTL memory, we propose that CTL memory may have evolved in order to clear the virus during primary challenge. W e show experimental data from lymphocytic choriomeningitis virus infection in mice, supporting our theory on CTL memory. We adapt our models to HIV and find that immune impairment during the primary phase of the infection may result in the failure to establish CTL memory which in turn leads to viral persistence. Based on our ...

Legal documents and investigative reports can be deadly reading, but the U.S. Anti-Doping Agencys 202-page report released Wednesday documenting its case against former cyclist Lance Armstrong is as good as any spy novel.. The report was posted in its entirety on The New York Times website, and it was heralded as the most extensive, groundbreaking layout of Armstrongs alleged doping, bolstered by new interviews, financial statements and laboratory results.. Within the first 25 pages, the investigation details Lance Armstrongs alleged rendezvous with drug suppliers on Europes back roads, and saline IVs used before a drug test to mask results. Its juicy stuff, regardless of your pro- or anti-Lance views. It includes sworn statements from more than 24 witnesses, 15 professional cyclists, including 11 former Armstrong teammates and, adding more intrigue, an interview with a masseuse.. The USADA is the latest government agency to come after Armstrong, who has so far successfully fought off any ...

PENSACOLA, Fla. - Top-ranked Armstrong Atlantic State advanced in penalty kicks, 6-5, past No. 19 Columbus State University on Friday afternooon, capturing the NCAA Division II Womens Soccer Southeast Region title and setting up a showdown with nationally-ranked No. 2 West Florida in the NCAA Quarterfinals on Sunday. The two teams played to a scoreless draw prior to PKs.. It was the first PK shootout win for Armstrong (19-1-2) in program history and keeps the Pirates drive towards a return trip to the Final Four alive. Columbus State (18-3-2) sees its season end on PKs in the NCAA Tournament for a third time in its history.. A tight defensive struggle between both teams generated just five shots between the two teams in the first half. The game opened up a little bit in the second half as each goalkeeper, Mary Mancin for Columbus State and Morgan Luckie for Armstrong, was called upon to make saves to preserve the shutout.. As time ran down in regulation, Columbus States Jackie Ellis had a ...

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In a series of emails to media organistions and cycling officials disgraced former Tour de France winner Floyd Landis yesterday admitted to systematic doping and implicated a number of other riders too including arguably cyclings biggest ever star, Lance Armstrong.. Amongst those emailed were the Wall Street Journal, it has been able to confirm to its satisfaction that the emails were genuinely from Landis - the newspaper has taken nearly three weeks to go public on the mails. That Landis doped is not a surprise, that he has finally admitted it is something of a bombshell given the loud and long campaign he waged, and which was waged by many on his behalf in the US media, to proclaim his innocence.. That particuar bombshell pales in to insignificance compared to what Landis has to say about his fellow American and erstwhile team mate, Lance Armstrong. However Armstrong, who has so far seemed to laugh off the accusations in allusions to them on his Twitter page, is not the only American rider ...

Armstrong State University is now Georgia Southern University. For information about Fall 2018 and beyond, visit GeorgiaSouthern.edu. Current Armstrong students (spring and summer 2018) can continue to access information through Armstrong.edu. For details about the consolidation, visit consolidation.georgiasouthern.edu ...

Armstrong State University is now Georgia Southern University. For information about Fall 2018 and beyond, visit GeorgiaSouthern.edu. Current Armstrong students (spring and summer 2018) can continue to access information through Armstrong.edu. For details about the consolidation, visit consolidation.georgiasouthern.edu ...

Dr. David Armstrong, MD is a Colorectal Surgery Specialist in Alpharetta, GA. Dr. Armstrong has more experience with Colorectal Surgery and Transplant Surgery than other specialists in his area. He is affiliated with medical facilities such as Emory Decatur Hospital and Emory University Hospital Midtown. He is accepting new patients and has indicated that he accepts telehealth appointments. Be sure to call ahead with Dr. Armstrong to book an appointment.

PubMed journal article: Development of a reverse transcription-polymerase chain reaction assay for diagnosis of lymphocytic choriomeningitis virus infection and its use in a prospective surveillance study. Download Prime PubMed App to iPhone, iPad, or Android

The primary finding of this study was the emergence of a distinct A-to-G/U-to-C hypermutation pattern in the single-stranded RNA genome of LCMV both in cell culture and in the organs of infected mice. This pattern is probably due to unspecific deamination by ADAR1-L, which was found to be upregulated during infection of cells and mice with LCMV. Furthermore, these A-to-G mutations lead to a high percentage of nonfunctional viral protein, thereby weakening viral fitness.. The A-to-G hypermutation pattern observed in this study was most likely attributed to RNA editing and not to errors of the viral polymerase. The hypermutation pattern was not observed 2 days after infection in L929 cells. In mice at days 5 and 8 p.i., the dominance of A-to-G mutations is also reduced compared to that at day 4, which is consistent with lower ADAR1-L expression at these time points. Furthermore, although viral RNA polymerases lack 3′-to-5′ proofreading activity, they have never been reported to exhibit a ...

During chronic stimulation, CD8+ T cells acquire an exhausted phenotype characterized by expression of inhibitory receptors, down-modulation of effector function, and metabolic impairments. T cell exhaustion protects from excessive immunopathology but limits clearance of virus-infected or tumor cells. We transcriptionally profiled antigen-specific T cells from mice infected with lymphocytic choriomeningitis virus strains that cause acute or chronic disease. T cell exhaustion during chronic infection was driven by high amounts of T cell receptor (TCR)-induced transcription factors IRF4, BATF, and NFATc1. These regulators promoted expression of inhibitory receptors, including PD-1, and mediated impaired cellular metabolism. Furthermore, they repressed the expression of TCF1, a transcription factor required for memory T cell differentiation. Reducing IRF4 expression restored the functional and metabolic properties of antigen-specific T cells and promoted memory-like T cell development. These ...

Persistent viral infections can interfere with FcγR-mediated antibody effector functions by excessive immune complex (IC) formation, resulting in resistance to therapeutic FcγR-dependent antibodies. We and others have previously demonstrated that mice persistently infected with lymphocytic choriomeningitis virus (LCMV) are resistant to a wide range of depleting antibodies due to excessive IC formation. Here, we dissect the mechanisms by which two depleting antibodies overcome the obstacle of endogenous ICs and achieve efficient target cell depletion in persistently infected mice. Efficient antibody-mediated depletion during persistent LCMV infection required increased levels of antibody bound to target cells or use of afucosylated antibodies with increased affinity for FcγRs. Antibodies targeting the highly expressed CD90 antigen or overexpressed human CD20 efficiently depleted their target cells in naïve and persistently infected mice, whereas antibodies directed against less abundant ...

Dendritic cells (DCs) comprise the major antigen-presenting cells (APCs) of the host, uniquely programmed to stimulate immunologically naïve T lymphocytes. Viruses that can target and disorder the...

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