Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mice could be significantly protected against infection with herpes simplex virus (HSV) by i.p. or i.v. injection of killed Corynebacterium parvum 7 days before infection. This protection was seen in inbred strains of mice with a different degree of sensitivity to HSV and after both i.p. and i.v. infection. Resistant mice immunosuppressed by X-irradiation and showing an increased susceptibility to HSV could also be protected by a previous injection of C. parvum. Elevated levels of interferon were demonstrated in the serum of mice injected with C. parvum 5 to 12 days previously. Four different strains of anaerobic coryneforms were compared and only those which were able to induce a systemic activation of the lymphoreticular system (as reflected by splenomegaly) protected against HSV infection. Protection against HSV-infection could also be demonstrated by using killed Bordetella pertussis. C. parvum also protected against Semliki Forest virus infection in two different strains of mice.
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PMID:Protection of mice against viral infection by Corynebacterium parvum and Bordetella pertussis. 21 22

SN11841 [4'-(9-acridinylamino)-methanesulfon-m-aniside] is an antitumor compound discovered by B.F. Cain. The LD50 for BALB/c mice with single intraperitoneal dosage is approximately 25 mg/kg. RLV-(Rauscher leukemia virus)-induced splenomegaly, a disease indicator in BALB/c mice, is inhibited at SN11841 doses not causing acute mortality. The life span of RLV-infected mice increases at some SN11841 doses. SN11841 does not have direct, or virolytic effects on RLV under conditions approximating those of antiviral effectiveness. SN11841 is cytotoxic for cells in tissue culture, as measured by inhibition of growth rate or vital dye uptake. At nontoxic concentrations SN11841 has no effect on RLV infectivity for murine cells, as determined by XC-cell induced syncytium formation. SN11841 has antiviral activity against vaccinia virus in tissue culture but is inactive against herpes simplex (Type 1), vesicular stomatitis, encephalomyocarditis, or reoviruses. SN11841 apparently does not act by inducing interferon. SN11841 is chemically labile, particularly in the presence of sulfhydryl compounds, but the degradation products resulting from prolonged storage in media are neither cytotoxic nor antiviral.
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PMID:Antiviral activities of 4'-(9-acridinylamino)-methanesulfon-M-aniside (SN11841). 28 Jan 45

Murine acquired immunodeficiency syndrome (MAIDS) was induced in C57BL/6 mice following infection with the LP-BM5 retrovirus complex. Infected mice developed splenomegaly, lymphadenopathy and loss of B- and T-cell functions 100 days after virus inoculation. Mice with AIDS were highly susceptible to opportunistic murine cytomegalovirus (MCMV) and herpes simplex virus (HSV-1) infections. The therapeutic activities of two phosphonylmethoxyalkyl derivatives, 9-(2-phosphonylmethoxyethyl)adenine (PMEA) and (S)-1-(3-hydroxy-2-phosphonylmethoxy-propyl)cytosine (HPMPC), were evaluated in MAIDS immunosuppressed mice infected with MCMV or HSV-1. MCMV infection resulted in extensive viral replication in lung, liver and spleen and death occurred five to twelve days post-infection. Treatment with either HPMPC or ganciclovir (DHPG) reduced mortality and viral replication in target organs; however, HPMPC was as effective as DHPG at one-fifth the DHPG dose. Moreover, when a single dose (100 mg/kg) of HPMPC was administered 24 h prior to MCMV infection, it suppressed virus replication at seven and 14 days post-infection, thus resulting in a significant prolongation of life. PMEA was effective against opportunistic HSV-1 infections, but appeared to be less effective than HPMPC against MCMV infections. These results indicate that MAIDS can be used as a model for evaluating antivirals in an immunocompromised host, and suggest that both PMEA and HPMPC may be useful in the treatment of opportunistic CMV and HSV-1 infections.
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PMID:Phosphonylmethoxyalkyl purine and pyrimidine derivatives for treatment of opportunistic cytomegalovirus and herpes simplex virus infections in murine AIDS. 166 26

Sore throats are most commonly due to infections, many of which are viral and do not require specific treatment. Symptoms and signs of the common cold, influenza or croup, the occurrence of conjunctivitis in some adenoviral infections, generalised lymphadenopathy and splenomegaly in glandular fever or the presence of vesicles characteristic of herpangina (Coxsackie A virus) or of herpes simplex infection, occasionally enable a clinical diagnosis and avoid the need for antibiotic therapy. In the case of treatable conditions a typical membrane may suggest diphtheria, a scarlatiniform rash infection due to Streptococcus pyogenes or to Corynebacterium haemolyticum, and a cherry-red epiglottis Haemophilus influenzae type b. Associated atypical pneumonia suggests infection with Mycoplasma pneumoniae or Chlamydia pneumoniae. Pharyngitis due to Neisseria gonorrhoeae may be accompanied by infection at other sites or by other sexually transmitted diseases. Candidal infection, in the appropriate clinical circumstance, should suggest HIV infection. Surgical drainage is required in the case of peritonsillar or retropharyngeal abscess. Noninfectious cases of sore throat, e.g. thyroiditis, are relatively uncommon considerations in the differential diagnosis of acute febrile pharyngitis. The most common problem is to recognise streptococcal pharyngitis, which requires antibiotic treatment for 10 days to avoid the risk of rheumatic fever.
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PMID:The sore throat. When to investigate and when to prescribe. 207

Time-pregnant Sprague-Dawley rats were injected subcutaneously with 20 mg/kg of cocaine HCl or 0.9% saline daily from gestation days 15 through 21. Maternal plasma levels of approximately 720 ng/ml of cocaine did not alter maternal weight gain during treatment, duration of pregnancy, any of the litter variables or several indices of maternal behavior. Offsprings' body weight from birth to 30 days of age and physical maturation were not generally affected by prenatal cocaine exposure. While the development of surface righting, cliff avoidance, and the startle response was accelerated in cocaine-exposed offspring, acquisition of a preference for a social odor was unaltered. Prenatal cocaine also attenuated the locomotor response of the offspring to d-amphetamine and cocaine at PND 15; at PND 30 both of these catecholaminergic agonists increased activity in prenatal saline and prenatal cocaine offspring. However, the difference in plasma levels of cocaine at PND 30 suggests a possible down-regulation of adrenergic receptors following prenatal cocaine exposure. Decreased thymus/body weight ratios and splenomegaly were observed in prenatal cocaine animals at 55 days of age. Although complete neutralization of herpes simplex virus-type 1 was not observed, sera from prenatal cocaine offspring showed an increased rate of appearance of cytopathic effect, while sera from animals given cocaine postnatally showed a reduction in the rate at which viral infectivity was expressed in culture. These results indicate that prenatal cocaine exposure can alter neurobehavioral ontogeny and humoral immune responsitivity in the offspring.
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PMID:Neurobehavioral and immunological effects of prenatal cocaine exposure in rat. 216 88

Effects of dietary vitamin B6 at levels ranging from deficiency to megadoses on the development of herpes simplex virus type 2-transformed (H238) cell-induced tumors and on in vitro responses relating to cell-mediated immunity were examined. Male BALB/cByJ mice (n = 260), 5 weeks of age, were fed 20% casein diets containing pyridoxine (PN) at 0.2, 1.2 for the control diet, 7.7, or 74.3 mg/kg diet for 4-11 weeks. After 4 weeks of dietary treatment, 120 of the mice received an injection of H238 cells; mice without H238 injection served as controls. At 4, 8, and 11 weeks, animals from each group were euthanized and blood and spleen samples obtained. Mice fed 0.2 mg PN developed mild deficiency symptoms and gained significantly less weight than those fed 1.2-, 7.7-, and 74.3-mg PN diets. Thirteen to 16 days after tumor cell injection, primary tumor incidence was lowest in mice fed 74.3 mg PN; later, incidence among groups was similar. Mice fed 1.2 mg PN had the largest primary tumor volume, the highest incidence of lung metastases, and the greatest number of metastatic nodules per animal at 7 weeks post injection. Overall, lower tumor volumes were found in animals fed 7.7 and 74.3 mg PN (14 and 32% less than the tumor volume for those fed 1.2 mg PN, respectively); mice fed 0.2 mg PN had the lowest tumor volume. Blood and spleen lymphoproliferative response to stimulation by phytohemagglutinin or concanavalin A generally tended to be higher in mice fed 7.7 and 74.3 mg PN as compared to that in animals fed either 0.2 or 1.2 mg PN. However, decreased mitogen-stimulated responsiveness was observed in all animals with progressive tumor growth. Tumor growth also resulted in splenomegaly and increased thymic atrophy. Significant negative relationships between tumor volume and tumor pyridoxal 5-phosphate (PLP) concentrations were observed for 1.2-, 7.7-, and 74.3-mg PN diet groups. These data suggest that high dietary intake of vitamin B6 may have suppressed tumor development by either immune enhancement or PLP growth regulation of this tumor.
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PMID:Suppression of tumor growth and enhancement of immune status with high levels of dietary vitamin B6 in BALB/c mice. 347 3

A male patient, aged 23 years, with no notable previous history, was admitted to hospital because of fever, splenomegaly, and pancytopenia. The bone marrow was infiltrated by mature looking histiocytes displaying erythrophagocytosis. Other findings included polyclonal hypergammaglobulinemia, elevated transaminases, hypofibrinogenemia, and hypertriglyceridemia. A diagnosis of virus-associated hemophagocytic syndrome was made and virology studies attributed it to herpes simplex virus type 1. Therapy with acyclovir, high dose i.v. immunoglobulins, and vinblastine was unsuccessful. With the addition of prednisone, a remission, with disappearance of histiocytic marrow involvement, was obtained but was of short duration, and the outcome was fatal.
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PMID:[Hemophagocytic syndrome associated with herpes simplex virus. Apropos of a case with a fatal outcome]. 380 39

42 homosexual or bisexual men with persistent generalised lymphadenopathy not attributable to an identifiable cause have been followed longitudinally since February, 1981. Lymphadenopathy was accompanied by fatigue, low-grade fever and/or night sweats (57%), splenomegaly (29%), leucopenia (40%), hypergamma - globulinaemia (76%), and diminished proportion and absolute numbers of helper T cells (95%). Of the 26 patients who had lymph node biopsy, all showed benign reactive hyperplasia. After 15-30 (median 22) months, 8 patients have met criteria for the diagnosis of acquired immunodeficiency syndrome (AIDS). This outcome was associated with previous heavy nitrite inhalant use, with the presence of night sweats, with leucopenia, and with the triad of constitutional symptoms, splenomegaly, and leucopenia. In addition, a lower mean absolute helper T cell count and an increased frequency of anergy to mumps intradermal antigen and of herpes simplex virus isolation distinguished these patients from those remaining in the cohort, who seem to be stable and in some cases to have improved.
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PMID:Longitudinal study of persistent generalised lymphadenopathy in homosexual men: relation to acquired immunodeficiency syndrome. 614 74

When BALB/c mice were first infected with Rauscher murine leukemia virus (MuLV-R) and then superinfected with Herpes simplex virus type 2 (HSV-2) the inhibition of the evolution of splenomegaly was observed. The effect did not depend on the route of HSV-2 administration. Experiments in which potent anti-interferon serum was administered to double infected mice suggested that the antagonism between MuLV-R and HSV-2 was not mediated by endogenous interferon, HSV-2 was found to replicate in the LPS stimulated spleen cells which are also target cells for MuLV-R; this suggested that the intrinsic interference between both viruses could take place. Mice with Rauscher virus induced disease were found to be more susceptible to infection with Herpesviruses than normal mice.
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PMID:Double infection of BALB/c mice with Rauscher murine leukemia and Herpes simplex virus type 2. 625 90

The integrated proviral DNA of the polycythemia-inducing isolate of Friend spleen focus-forming virus (SFFVp) has been identified in rat cell clones nonproductively infected with this replication-defective erythroleukemia virus and cloned in phage lambda vectors. These lambda SFFVp recombinants, lambda SFFVp502 and lambda SFFVp542, contain endonuclease EcoRI inserts of size 7.4 and 8.2 kilobases, respectively, and include full copies of the SFFVp genome, along with host flanking sequences. Infectivity of the cloned SFFVp genomes was tested by a two-step DNA transfer procedure involving transfection of the cloned DNA into 3T3 mouse fibroblasts or cotransfer of the cloned DNA into thymidine kinase-deficient 3T3 cells together with the cloned thymidine kinase gene of herpes simplex virus, followed by rescue of the transferred DNA by superinfection with a helper virus. Inoculation of the rescued virus into adult mice resulted in the appearance of spleen foci, rapid splenomegaly, and polycythemia. Early after infection, spleen cell populations contained large numbers of cells capable of forming small erythroid colonies in vitro (CFU-E) in the absence of erythropoietin. Late after infection, these mice contained cells capable of forming macroscopic colonies (CFU-FV) in vitro. These data indicate that molecular clones of SFFVp, in conjunction with a helper virus, induce the appearance of hemopoietic colony-forming cells characteristic of both the early and late stages of Friend leukemia.
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PMID:Clonal analysis of early and late stages of erythroleukemia induced by molecular clones of integrated spleen focus-forming virus. 627 94


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