Damage to the nervous system associated with HIV infection (a clinical case)

In Eastern Europe, at least 130 thousand new cases of HIV infection have been registered, which undoubtedly reflects the urgency of this medical problem. In our country, the average rate of human immunodeficiency infection is 58 cases per 100 thousand people. It is known that the disease is caused by an RNA-containing human immunodeficiency virus. Two types of it have been studied — HIV-1 and HIV-2, which have many subtypes. An important clinical feature of this virus is its tropism to cells of the human nervous and immune systems. The main risk group for the disease is injecting drug users, blood recipients, and people with low social responsibility. The impairment of the nervous system in AIDS is represented by the AIDS-dementia complex, acute aseptic meningitis, HIV-associated myelopathy, pathology of the peripheral nervous system, as well as the influence of opportunistic infections and neoplasms. This article presents a clinical case of lesions of the nervous system associated with HIV infection and also considers the etiology, pathogenesis, features of the course, diagnosis, and treatment of patients with neuro-AIDS.

Neurocognitive profile of patients with early stages of HIV infection

HIV-associated neurocognitive disorders (HAND) may include neurological disorders of various severities such as AIDS dementia complex (ADC) also known as HIV dementia and HIV-associated dementia (HAD), HIV encephalopathy, and Mild Neurocognitive Disorder (MND). As it seems HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. Despite of a group, evidences have described presence of cognitive alterations in HIV patients at different stages of HIV infection so far; little is known about the neurocognitive state of patients at very early stages of HIV infection. Here, we explored the neurocognitive profile of a group of cases of HIV patients at very early stages of HIV infection. We have analyzed of three groups of subjects, thus, we have studied a group of patients with early HIV infection, a healthy control group and a group of patients with mild cognitive impairment due to neurodegenerative causes. Our results suggested that cognitive processes are sensitive to very early neuropathological changes in HIV infection. Noteworthy, our results also showed that neurocognitive profile of HIV patients differs from those cognitive alterations in patients with mild cognitive disorders associated to primary neurodegeneration. Together, our results point out that HIV infection generates neural changes even at early stages of infection. Furthermore, our results highlight the importance of a deep neurocognitive exploration at very early stages of HIV infection as this approach allow improve the accompaniment, clinical attachment and interventions.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Design and Pharmaceutical Evaluation of a Nano-Enabled Crosslinked Multipolymeric Scaffold for Prolonged Intracranial Release of Zidovudine

Purpose. Nanomedicine explores and allows for the development of drug delivery devices with superior drug uptake, controlled release and fewer drug side-effects. This study explored the use of nanosystems to formulate an implantable drug delivery device capable of sustained zidovudine release over a prolonged period. Methods. Pectin and alginate nanoparticles were prepared by applying a salting out and controlled gelification approach, respectively. The nanoparticles were characterized by attenuated total reflectance-fourier transform infrared spectroscopy (ATR-FTIR), scanning electron microscopy (SEM), transmission electron microscopy (TEM) and dynamic light scattering (DLS) and were further evaluated for zidovudine (AZT) entrapment efficiency. Multipolymeric scaffolds were prepared by crosslinking carboxymethyl cellulose, polyethylene oxide and epsilon caprolactone for entrapment of zidovudine-loaded alginate nanoparticles to impart enhanced controlled release of zidovudine over the time period. Swelling and textural analysis were conducted on the scaffolds. Prepared scaffolds were treated with hydrochloric acid (HCl) to reduce the swelling of matrix in the hydrated environment thereby further controlling the drug release. Drug release studies in phosphate buffered saline (pH 7.4, 37°C) were undertaken on both zidovudine-loaded nanoparticles and native scaffolds containing alginate nanoparticles. Results. A higher AZT entrapment efficiency was observed in alginate nanoparticles. Biphasic release was observed with both nanoparticle formulations, exhibiting an initial burst release of drug within hours of exposure to PBS, followed by a constant release rate of AZT over the remaining 30 days of nanoparticle analysis. Exposure of the scaffolds to HCl served to reduce the drug release rate from the entrapped alginate nanoparticles and extended the AZT release up to 30 days. Conclusions. The crosslinked multipolymeric scaffold loaded with alginate nanoparticles and treated with 1% HCl showed the potential for prolonged delivery of zidovudine over a period of 30 days and therefore may be a potential candidate for use as an implantable device in treating Aids Dementia Complex. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.