The nervous system in early HIV infection: a prospective study through 7 years

Samuelsson, Karin; Pirskanen-Matell, R.; Bremmer, Staffan; Hindmarsh, T; Nilsson, Björn M.; Persson, Hans

doi:10.1111/j.1468-1331.2006.01173.x

Cited by 19 publications

(10 citation statements)

References 33 publications

(43 reference statements)

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“…20 The severity of symptoms varies, however; in a study of 28 patients with early stage HIV infection (CD4 >280 cells/mm 3 ), not receiving HAART, and followed during 7 years, no major deterioration in the neurological, psychological performance, neurophysiological or neuroimaging examinations could be revealed. 27 Elevated HIV RNA in CSF may predict subsequent progression to neuropsychological impairment. 28 Amyotrophic lateral sclerosis (ALS)-like syndrome can occur in association with HIV infection 29 , as well as sensory neuropathies 30 , and neuromuscular syndromes as distal symmetric polyneuropathy (DSP), myopathy and HIVassociated neuromuscular weakness syndrome.…”

Section: 7mentioning

confidence: 99%

HIV infection and psychiatric illness

Owe‐Larsson

Säll²,

Salamon³

et al. 2009

Afr. J. Psych

139

125

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Introduction HIV is a ribonucleic acid (RNA) retrovirus that is the causative agent for AIDS. HIV belongs to the Lentivirus genus in the family Retroviridae, characterized by a replication cycle in which the viral RNA is reverse transcribed into a DNA proviral form that is integrated into the host cell genome. The retrovirus is composed of two copies of single-stranded RNA that codes for the virus's 9 genes. The RNA is non-covalently linked to the core proteins, which in turn is surrounded by a viral envelope, which enables the virus to enter cells by binding to a specific cellular receptor located on the surface of cluster of differentiation 4 (CD4) cells. 1 A few years after the discovery of HIV-1, a second virus, HIV-2, was found in West Africa. HIV-1 and HIV-2 differ regarding their content of the genome, resulting in lower AIDS rates in HIV-2 infected individuals. 2 Once exposed to the body, the HIV virus antibodies may be detected after an acute flu-like illness, and then proceeds to infect specific cells of the immune system during an asymptomatic period that may last for years. In order to enter a cell, HIV must bind to CD4, typically found on T lymphocytes, blood monocytes, macrophages and some dendrite cells, and subsequently to one or a combination of several possible chemokine co-receptors, usually CCR5 and CXCR4. 3,4 The late HIV infection and psychiatric illness B Owe-Larsson, L Säll, E Salamon, C Allgulander Karolinska Institutet, Department of Clinical Neuroscience, Section of Psychiatry at Karolinska University Hospital Huddinge, Stockholm, Sweden Abstract Objective: To review the clinical features and current knowledge on the treatment of psychiatric symptoms and disorders in patients with human immunodeficiency virus (HIV) infection. Method: We searched the PubMed database combining HIV/AIDS with different keywords for psychiatric diagnoses and symptoms (e.g. depression, mania, anxiety, psychosis, dementia, substance abuse) and for psychopharmacological treatment. The years covered by these searches included 1980 to 2008. Results: Patients with HIV infection are at an increased risk of psychiatric illness. Major depressive disorder and subsyndromal depressive symptoms, as well as anxiety disorder and substance abuse are more prevalent among HIV infected individuals than among the general population. HIV-associated neurocognitive disorders (HAND) are common among HIV patients, and HIV-associated dementia (HAD) is a serious condition during the acquired immune deficiency syndrome (AIDS) stage of HIV disease. Secondary mania and psychosis might be the first clinical symptom of HIV dementia. The introduction of highly active anti-retroviral therapy (HAART) has resulted in significant decreases in morbidity and mortality for HIV infected patients. HAART has also decreased the incidence of HAD, but does not give complete protection from this condition. The utility of psychotropic medications in HIV patients has not been studied sufficiently as a basis for guidelines, and more controlled trials are n...

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Section: 7mentioning

confidence: 99%

HIV infection and psychiatric illness

Owe‐Larsson

Säll²,

Salamon³

et al. 2009

Afr. J. Psych

139

125

View full text Add to dashboard Cite

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“…The recording of the auditory evoked potentials is a method for studying the function and integrity of the auditory pathway during the early stages of neurological disorders, including HIV (Samuelsson et al, 2006). The BAEP is the most commonly studied of all auditory potentials and it reflects the transmission time of stimuli along the brainstem portion of the primary auditory pathway.…”

Section: Discussionmentioning

confidence: 99%

Strain-specific viral distribution and neuropathology of feline immunodeficiency virus

Miller

Bielefeldt‐Ohmann

MacMillan

et al. 2011

Veterinary Immunology and Immunopathology

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Feline immunodeficiency virus (FIV) is a naturally-occurring lentivirus of domestic cats, and is the causative agent of feline AIDS. Similar to human immunodeficiency virus (HIV), the pathogenesis of FIV involves infection of lymphocytes and macrophages, and results in chronic progressive immune system collapse and death. Neuropathologic correlates of FIV infection have not yet been elucidated, and may be relevant to understanding HIV-associated neurologic disease (neuroAIDS). As in HIV, FIV strains have been shown to express differential tendencies towards development of clinical neuroAIDS. To interrogate viral genetic determinants that might contribute to neuropathogenicity, cats were exposed to two well-characterized FIV strains with divergent clinical phenotypes and a chimeric strain as follows: FIVPPR (PPR, relatively apathogenic but associated with neurologic manifestations), FIVC36 (C36, immunopathogenic but without associated neurologic disease), and Pcenv (a chimeric virus consisting of a PPR backbone with substituted C36 env region). A sham inoculum control group was also included. Peripheral nerve conduction velocity, CNS imaging studies, viral loads and hematologic analysis were performed over a 12 month period. At termination of the study (350 days post-inoculation), brain sections were obtained from four anatomic locations known to be involved in human and primate lentiviral neuroAIDS. Histological and immunohistochemical evaluation with seven markers of inflammation revealed that Pcenv infection resulted in mild inflammation of the CNS, microglial activation, neuronal degeneration and apoptosis, while C36 and PPR strains induced minimal neuropathologic changes. Conduction velocity aberrations were noted peripherally in all three groups at 63 weeks post-infection. Pcenv viral load in this study was intermediate to the parental strains (C36 demonstrating the highest viral load and PPR the lowest). These results collectively suggest that (i) 3′ C36 genomic elements contribute to viral replication characteristics, and (ii) 5′ PPR genomic elements contribute to CNS manifestations. This study illustrates the potential for FIV to provide valuable information about neuroAIDS pathogenesis related to genotype and viral kinetics, as well as to identify strains useful to evaluation of therapeutic intervention.

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“…Furthermore, to characterize the type of encephalopathy (e.g. HIV‐E) a finger tapping test, verbal fluency, trail making A and B, as well as a digit symbol test were performed, as described earlier [12].…”

Section: Methodsmentioning

confidence: 99%