scholarly journals Racemose Pattern of Intracranial Tuberculoma at the Basal, Suprasellar and Perimesencephalic Cisterns – A Case Report

2020 ◽  
pp. 1-4
Author(s):  
Saumitra Sarkar ◽  
Sarkar S ◽  
Saumitra Sarkar ◽  
A Dey ◽  
MMH Morshed
Keyword(s):  
Human Immunodeficiency Virus ◽  
Clinical Symptoms ◽  
Miliary Tuberculosis ◽  
Developed Countries ◽  
Common Site ◽  
Intracranial Tuberculoma ◽  
Immunodeficiency Virus ◽  
Radiological Abnormality ◽  
Subarachnoid Spaces ◽  
The Brain

Central nervous system tuberculosis may present as meningitis, tuberculoma, abscesses, cerebritis or miliary tuberculosis. The most common site of tuberculoma has been reported to be at the grey-white matter junction and the periventricular region. They may even be found in the epidural, subdural and subarachnoid spaces, and the brain stem. Although tuberculosis is very common in developing countries, with the increasing prevalence of immunosuppression owing to human immunodeficiency virus and patients surviving chemotherapy or organ transplantation, the incidence of tubercular infections has been rising in developed countries. The authors report a 15-year-old boy of intracranial tuberculoma at the basal, suprasellar and perimesencephalic cisterns in a patient. Tuberculous involvement was noted in a racemose pattern in the subarachnoid space. The patient’s clinical symptoms resolved with no recurrence of symptoms but only persistence of the radiological abnormality after antitubercular chemotherapy.

Human Immunodeficiency Virus and Artificial Feeding

PEDIATRICS ◽  
1989 ◽  
Vol 83 (5) ◽  
pp. 804-804
Author(s):  
STANLEY A. PLOTKIN
Keyword(s):  
United States ◽  
Human Immunodeficiency Virus ◽  
Developing Countries ◽  
Breast Milk ◽  
Infection Control ◽  
Hiv Infection ◽  
Developed Countries ◽  
The United States ◽  
Artificial Feeding ◽  
Immunodeficiency Virus

Dr Halsey has brought to my attention that a sentence in the human immunodeficiency virus (HIV) infection control statement (AAP News, September 1988) and perinatal statement (Pediatrics 1988;82:941-944) might be misinterpreted as advocating artificial feeding for HP/-infected infants in developing countries. It was our intention to advocate the use of artificial feeding by HIV-infected mothers only in the United States and other developed countries where safe water and hygienic practices are the norm. In other countries, the advantages of breast milk outweigh the possible risk of transmission to the newborn.

Cellular immune activation in the brain and human immunodeficiency virus infection

1988 ◽  
Vol 24 (2) ◽  
pp. 289-289 ◽  
Author(s):  
Dietmarch Fuchs ◽  
Ernst R. Werner ◽  
Manfred P. Dierich ◽  
Helmut Wachter
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
Immune Activation ◽  
Immunodeficiency Virus ◽  
Cellular Immune ◽  
The Brain

History of Human Immunodeficiency Virus Infection and the Nervous System

2017 ◽  
Author(s):  
Avindra Nath
Keyword(s):  
Human Immunodeficiency Virus ◽  
Nervous System ◽  
Hiv Infection ◽  
System P ◽  
Clinical Syndromes ◽  
Tremendous Progress ◽  
Immunodeficiency Virus ◽  
History Of ◽  
The Brain ◽  
First Descriptions

It has been nearly three decades since the first descriptions of the neurological comploications of HIV infection. During this period of time there has been tremendous progress in defining the clinical syndromes, modes of diagnosis, detailed pathophysiology and modes of treatment. Many of the dreaded complications are now manageable particularly if diagnosed early. However, neurocognitive impairment associated with HIV infection still remains a significant cause of morbidity and much is needed to control; the effects of the virus on the brain and for the eventual eradication of the virus from the brain reservoir.

Human Immunodeficiency Virus and the Brain: Investigation of Virus Load and Neuropathologic Changes in Pre-AIDS Subjects

1993 ◽  
Vol 168 (4) ◽  
pp. 818-824 ◽  
Author(s):  
J. E. Bell ◽  
A. Busuttil ◽  
J. W. Ironside ◽  
S. Rebus ◽  
Y. K. Donaldson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Load ◽  
Immunodeficiency Virus ◽  
The Brain

scholarly journals Effects of Tat proteins and Tat mutants of different human immunodeficiency virus type 1 clades on glial JC virus early and late gene transcription

2013 ◽  
Vol 94 (3) ◽  
pp. 514-523 ◽  
Author(s):  
Clayton A. Wright ◽  
Jonas A. Nance ◽  
Edward M. Johnson
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Replication ◽  
Gene Transcription ◽  
Cellular Proteins ◽  
Late Gene ◽  
Clade B ◽  
Immunodeficiency Virus ◽  
The Brain ◽  
Hiv 1

Polyomavirus JC (JCV) is the aetiological agent of progressive multifocal leukoencephalopathy (PML), a frequently fatal infection of the brain afflicting nearly 4 % of AIDS patients in the USA. Human immunodeficiency virus type 1 (HIV-1) Tat, acting together with cellular proteins at the JCV non-coding control region (NCCR), can stimulate JCV DNA transcription and replication. Tat in the brain is secreted by HIV-1-infected cells and incorporated by oligodendroglia, cells capable of infection by JCV. Thus far the effects of Tat on JCV have been studied primarily with protein encoded by the HIV-1 B clade most common in North America. Here, we determine the abilities of Tat from different HIV-1 clades to alter JCV early and late gene transcription and DNA replication initiated at the JCV origin. Tat from all clades tested stimulates both JCV early and late gene promoters, with clade B Tat being significantly most effective. Tat proteins from the HIV-1 clades display parallel patterns of differences in their effects on HIV-1 and JCV transcription, suggesting that Tat effects in both cases are mediated by the same cellular proteins. Clade B Tat is most effective at directing Smad mediators of tumour growth factor beta and cellular partner Purα to the NCCR. Tat proteins from all non-B clades inhibit initiation of JCV DNA replication. The effectiveness of HIV-1 clade B Tat at promoting JCV transcriptional and replicative processes highlights a need for further investigation to determine which molecular aspects of Tat from distinct HIV-1 substrains can contribute to the course of PML development in neuroAIDS.

scholarly journals Human Immunodeficiency Virus Type 1 Infection Increases the In Vivo Capacity of Peripheral Monocytes To Cross the Blood-Brain Barrier into the Brain and the In Vivo Sensitivity of the Blood-Brain Barrier to Disruption by Lipopolysaccharide

2008 ◽  
Vol 82 (15) ◽  
pp. 7591-7600 ◽  
Author(s):  
Hongwei Wang ◽  
Jinglin Sun ◽  
Harris Goldstein
Keyword(s):  
Human Immunodeficiency Virus ◽  
Blood Brain Barrier ◽  
Human Immunodeficiency Virus Type ◽  
Brain Barrier ◽  
Blood Brain ◽  
Immunodeficiency Virus ◽  
The Brain ◽  
Hiv 1

ABSTRACT Human immunodeficiency virus type 1 (HIV-1), introduced into the brain by HIV-1-infected monocytes which migrate across the blood-brain barrier (BBB), infects resident macrophages and microglia and initiates a process that causes HIV-1-associated neurocognitive disorders. The mechanism by which HIV-1 infection circumvents the BBB-restricted passage of systemic leukocytes into the brain and disrupts the integrity of the BBB is not known. Circulating lipopolysaccharide (LPS), which can compromise the integrity of the BBB, is significantly increased in HIV-1-infected individuals. We hypothesized that HIV-1 infection increases monocyte capacity to migrate across the BBB, which is further facilitated by a compromise of BBB integrity mediated by the increased systemic LPS levels present in HIV-1-infected individuals. To investigate this possibility, we examined the in vivo BBB migration of monocytes derived from our novel mouse model, JR-CSF/EYFP mice, which are transgenic for both a long terminal repeat-regulated full-length infectious HIV-1 provirus and ROSA-26-regulated enhanced yellow fluorescent protein. We demonstrated that JR-CSF/EYFP mouse monocytes displayed an increased capacity to enter the brain by crossing either an intact BBB or a BBB whose integrity was partially compromised by systemic LPS. We also demonstrated that the JR-CSF mouse BBB was more susceptible to disruption by systemic LPS than the control wild-type mouse BBB. These results demonstrated that HIV-1 infection increased the ability of monocytes to enter the brain and increased the sensitivity of the BBB to disruption by systemic LPS, which is elevated in HIV-1-infected individuals. These mice represent a new in vivo system for studying the mechanism by which HIV-1-infected monocytes migrate into the brain.

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