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At least 289 records · Page 16Linked to original sources
PubMed1975

The effect of supraoptimal temperature on the multiplication of different cytomegalovirus strains.

The virion synthesis by five human cytomegalovirus (CMV) strains in human embryonic fibroblast cultures was stopped by incubation of the infected cultures at 40 degrees C. At this temperature the antigens appeared diffusely filling the nucleus and the cytoplasm. The blocking effect of the elevated temperature was exerted in the same period of the reproduction cycle as the inhibitory effect of cytosine arabinoside (ara-C). In cell cultures infected with CMV and incubated first at 40 degrees C, then at 37 degrees C, the synthesis of infectious virus started again, thus the abortive cycle developed at 40 degrees C was reversible. The inhibition of virus multiplication cannot be attributed to the thermosensitive events in the normal function of the host cell.

Antigens, Viral↗
PubMedDate not supplied

Postabortal infectious morbidity after antibiotic treatment of chlamydia-positive patients.

The postabortal infection rate in chlamydia-positive women after antibiotic treatment (doxycycline or erythromycin) was compared with infectious morbidity among untreated culture-positive women in a comparable previous study. Of 69 chlamydia-positive patients, 5 (7.2%) developed endometritis and one (1.4%) salpingitis during the first postoperative month. The corresponding figures during the previous regimen were 16 (23.2%) and 10 (14.5%), respectively, i.e. a highly significant decrease (P less than 0.001). The infection rate among the chlamydia-negative women was unchanged. It is suggested that preoperative screening for C. trachomatis should precede legal abortion. Initiation of treatment of culture-positive cases before or at least in conjunction with the abortion seems to reduce the risk of infectious complications to the same level as in chlamydia-negative women.

Abortion, Induced↗
PubMed2004

The health of young people in a global context.

PURPOSE: To examine the chief causes and influences of morbidity and mortality among young people throughout the world. METHODS: A comprehensive literature search was conducted that included WHO's Global Burden of Disease, UNFPA's State of the Worlds' Population, Medline, Popline, Sociological Abstracts, as well as data collected from UNICEF, UNAIDS, Population Reference Bureau, and the United Nations Headquarters. Experts in the fields of substance use, suicide, and infectious diseases were also contacted for unpublished and published sources. Studies were restricted to those completed after 1985, had a sample size of at least 100, focused primarily on the age group of 10-24 years, and examined trends related to unintentional injuries, HIV/AIDS, suicide, homicide, war, maternal mortality, pregnancy, abortion, sexually transmitted diseases, substance abuse, and infectious diseases. RESULTS: Trends in adolescent morbidity and mortality have shifted over the past decade from predominately infectious to social etiologies. Currently, unintentional injury is the leading killer of young people in nearly every region of the world, with homicide, war, and interpersonal violence following closely behind. CONCLUSIONS: The changes in population, migration, age of marriage, and education have had profound impact on the mortality and morbidity among adolescents. As we come to learn about the factors that influence adolescent morbidity and mortality, we begin to have a better understanding of how to improve the health of youth throughout the world.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Impaired interleukin 1 and interleukin 2 production following in vitro abortive infection of murine spleen mononuclear cells by Semliki Forest virus.

The effect of Semliki Forest virus (SFV) infection of murine spleen mononuclear cells was investigated in vitro. A small percentage of spleen macrophages expressed viral antigens, but no infectious virus particles were released, indicating an abortive-type infection. Wild-type SFV infected a higher percentage of macrophages than the attenuated, demyelinating mutant A7. The proliferation of spleen mononuclear cells under Con A stimulation was inhibited by the viral infection. The supernatant (SN) harvested from infected and Con A-stimulated spleen adherent cells could not stimulate thymocytes in an interleukin 1 (IL-1) assay and indomethacin treatment of infected cultures had no effect. The stimulatory effect of SN from noninfected cultures in the IL-1 assay was reduced when SN from infected cultures was added, suggesting the presence of an IL-1 inhibitor. Interleukin 2 (IL-2) production by splenocytes also decreased after viral infection, but exogenous IL-2 restored the response to Con A stimulation of infected spleen cells. This study demonstrates that abortive SFV infection of spleen macrophages has an immunosuppressive effect which may lead to an aberrant immune regulation.

Animals↗
PubMed1993

Recurrent spontaneous abortion: evaluation and management.

Recurrent, or habitual, spontaneous abortion may be related to anatomic, genetic, infectious, immunologic, endocrine, environmental or psychologic problems. A thorough evaluation of the possible etiologies may lead to an explanation, a therapy plan and a successful pregnancy. Psychosocial support is an integral part of both evaluation and treatment.

Abortion, Habitual↗
PubMed2001

HIV-1 penetrates coronary artery endothelial cells by transcytosis.

BACKGROUND: The pathogenesis of HIV-1-related cardiomyopathy is poorly understood, but HIV-1 has been detected in cardiomyocytes. Whether HIV-1 penetrates into the myocardium by infection of coronary artery endothelial cells (CAEC) or using transcellular or paracellular routes across CAEC has not been resolved. MATERIALS AND METHODS: A model of the CAEC barrier was constructed with primary CAEC (derived from human coronary vessels). Polymerase chain reaction (PCR) assay, infectious assay, and immunofluorescence were employed to show abortive nature of HIV-1 infection of CAEC. Tight junction (TJ) and cell adhesion proteins were visualized by immunofluorescence. The time course of HIV-1 invasion was measured by HIV-1 RNA assay. Inulin permeability assay determined paracellular leakage. Transmission electron microscopy demonstrated virus-induced endothelial vacuolization. RESULTS: Despite a strong display on CAEC of CXCR4 and a lesser expression of CCR3 and CCR5, HIV-1 did not productively replicate in CAEC, as shown by infectious assay, immunofluorescence, and electron microscopy. HIV-1 infection of CAEC was abortive with minimal reverse transcription of strong stop DNA and pol but not full-length or two LTR DNA circles. Upon infection of the model with 1 million RNA copies of HIV-1JR-FL, virus penetration 2 hr postinfection (PI) was negligible but increased by 1,750% 24 hr PI. The paracellular permeability increased during this period by only 25%. Neither AOP-RANTES nor v-MIPII significantly reduced HIV-1JR-FL invasion. Virus infection did not alter the integral TJ protein occludin and the TJ-associated protein ZO-1. HIV-1 exposed CAEC and brain microvascular endothelial cells (BMVEC) developed extensive cytoplasmic vacuolization with retroviral-like particles in the vacuoles. CONCLUSIONS: The endothelium is not an impenetrable barrier to HIV-1. The virus opens a transcellular route across coronary and brain endothelia in cytoplasmic vacuoles.

Arteries↗
PubMed1999

Tetanus and pregnancy-related mortality in Bangladesh.

A national survey of health-care providers in Bangladesh identified 298 women who died from pregnancy-related tetanus. Immunising all girls with tetanus toxoid and providing safe menstrual regulation services would prevent such deaths.

Abortion, Induced↗
PubMed2001

Infectious entry by amphotropic as well as ecotropic murine leukemia viruses occurs through an endocytic pathway.

Infectious entry of enveloped viruses is thought to proceed by one of two mechanisms. pH-dependent viruses enter the cells by receptor-mediated endocytosis and are inhibited by transient treatment with agents that prevent acidification of vesicles in the endocytic pathway, while pH-independent viruses are not inhibited by such agents and are thought to enter the cell by direct fusion with the plasma membrane. Nearly all retroviruses, including amphotropic murine leukemia virus (MuLV) and human immunodeficiency virus type 1, are classified as pH independent. However, ecotropic MuLV is considered to be a pH-dependent virus. We have examined the infectious entry of ecotropic and amphotropic MuLVs and found that they were equally inhibited by NH4Cl and bafilomycin A. These agents inhibited both viruses only partially over the course of the experiments. Agents that block the acidification of endocytic vesicles also arrest vesicular trafficking. Thus, partial inhibition of the MuLVs could be the result of virus inactivation during arrest in this pathway. In support of this contention, we found that that the loss of infectivity of the MuLVs during treatment of target cells with the drugs closely corresponded to the loss of activity due to spontaneous inactivation at 37 degrees C in the same period of time. Furthermore, the drugs had no effect on the efficiency of infection under conditions in which the duration of infection was held to a very short period to minimize the effects of spontaneous inactivation. These results indicate that the infectious processes of both ecotropic and amphotropic MuLVs were arrested rather than aborted by transient treatment of the cells with the drugs. We also found that infectious viruses were efficiently internalized during treatment. This indicated that the arrest occurred in an intracellular compartment and that the infectious process of both the amphotropic and ecotropic MuLVs very likely involved endocytosis. An important aspect of this study pertains to the interpretation of experiments in which agents that block endocytic acidification inhibit infectivity. As we have found with the MuLVs, inhibition of infectivity may be secondary to the block of endocytic acidification. While this strongly suggests the involvement of an endocytic pathway, it does not necessarily indicate a requirement for an acidic compartment during the infectious process. Likewise, a lack of inhibition during transient treatment with the drugs would not preclude an endocytic pathway for viruses that are stable during the course of the treatment.

3T3 Cells↗