Neurologic and neurodevelopmental manifestations of pediatric HIV/AIDS: A global perspective

Rie, Annelies Van; Harrington, Patrick R.; Dow, Anna; Robertson, Kevin

doi:10.1016/j.ejpn.2006.10.006

Cited by 151 publications

(129 citation statements)

References 108 publications

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“…The present model of HIV/AIDS has the greatest application to pediatric HIV/AIDS as it is a perinatal infection model, similar to what is observed in HIV-infected children (Van Rie et al, 2007). Hence an obvious strategy will be to extend the present findings to the clinical circumstances targeting the pediatric population with HIV infection, a group mostly neglected to date in terms of understanding the associated neuropathogenic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Neurobehavioral Performance in Feline Immunodeficiency Virus Infection: Integrated Analysis of Viral Burden, Neuroinflammation, and Neuronal Injury in Cortex

Maingat

Vivithanaporn²,

Zhu³

et al. 2009

Journal of Neuroscience

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Human immunodeficiency virus (HIV) infection causes motor and neurocognitive abnormalities affecting Ͼ50% of children and 20% of adults with HIV/AIDS (acquired immunodeficiency syndrome). The closely related lentivirus, feline immunodeficiency virus (FIV), also causes neurobehavioral deficits. Herein, we investigated the extent to which FIV infection affected specific motor and cognitive tasks in conjunction with viral burden and immune responses within the brain. Neonatal animals were infected with a neurovirulent FIV strain (FIV-Ch) and assessed in terms of systemic immune parameters, viral burden, neurobehavioral performance, and neuropathological features. FIV-infected animals displayed less weight gain and lower blood CD4 ϩ T-cell levels than mock-infected animals ( p Ͻ 0.05). Gait analyses disclosed greater gait width with increased variation in FIV-infected animals ( p Ͻ 0.05). Maze performance showed that FIV-infected animals were slower and made more navigational errors than mock-infected animals ( p Ͻ 0.05). In the object memory test, the FIV-infected group exhibited fewer successful steps with more trajectory errors compared with the mock-infected group ( p Ͻ 0.05). Performance on the gait, maze, and object memory tests was inversely correlated with F4/80 and CD3 expression ( p Ͻ 0.05) and with viral burden in parietal cortex ( p Ͻ 0.05). Amino acid analysis in cortex showed that D-serine levels were reduced in FIV-infected animals, which was accompanied by diminished kainate and AMPA receptor subunit expression ( p Ͻ 0.05). The neurobehavioral findings in FIV-infected animals were associated with increased gliosis and reduced cortical neuronal counts ( p Ͻ 0.05). The present studies indicated that specific motor and neurocognitive abilities were impaired in FIV infection and that these effects were closely coupled with viral burden, neuroinflammation, and neuronal loss.

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Section: Discussionmentioning

confidence: 99%

Neurobehavioral Performance in Feline Immunodeficiency Virus Infection: Integrated Analysis of Viral Burden, Neuroinflammation, and Neuronal Injury in Cortex

Maingat

Vivithanaporn²,

Zhu³

et al. 2009

Journal of Neuroscience

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“…The effect of HIV on an immature CNS (as in the case of vertically-infected infants) is injurious to a greater extent than in adults, where neurological impairments occur in 15-40% of all cases and manifest as progressive or static encephalopathy (Van Rie, et al, 2007, Belman, 1997. The effects of the virus on the CNS will differ according to the stage of brain development at time of infection (Belman, 1997), and this too, will lead to varying clinical presentations (Belman, 1990).…”

Section: The Developing Cns and Hivmentioning

confidence: 99%

“…HIV encephalopathy as a clinical diagnosis is the umbrella term given to the wide spectrum of presentations seen with CNS infection by HIV (Hilburn, et al, 2010;Sherr, et al, 2009;Van Rie, et al, 2007;Smith et al, 2006;Brouwers, et al, 1995;Chase, et al, 1995;Aylward, et al, 1992;Belman, 1992). It must be noted that there is a distinctly different pattern of clinical presentation seen in children when compared to the dementias seen in adults, due to the effect of the virus on an immature CNS (Smith, et al, 2006;Belman, 1997;Chase, et al, 1995 (WHO, p.37, 2007), which is not feasible for the majority of children living in developing countries.…”

Section: Clinical Manifestations Of Hiv Encephalopathymentioning

confidence: 99%

Developmental delay in HIV-exposed infants in Harare, Zimbabwe

Hutchings¹,

Potterton

2013

Vulnerable Children and Youth Studies

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The aim of this cross-sectional study was to determine the difference in development (cognition; receptive and expressive language; and fine and gross motor) of Human Immunodeficiency Virus (HIV) -exposed infected (HEI) infants with the development of HIV-exposed but uninfected (HEU) infants using the Bayley Scales of Infant and Toddler Development, Third Edition (BSID-III). Sixty infants were enrolled in the study; 32 (53.33%) HEU infants and 28 (46.67%) HEI infants. The two groups were well-matched for infant demographics, anthropometry at birth, maternal demographics, as well as socioeconomic status. Statistically significant differences were found in anthropometry and development between the HEI and HEU group. The HEI infants had malnutrition, were stunted and had smaller head circumferences than HEU infants. The BSID-III showed that the mean developmental delay for the HEI group was approximately two months below their mean chronological age for all scales (cognitive; receptive and expressive communication; and, fine and gross motor age).The HEI group showed that 64.29% had cognitive delay, 60.71% had language delay and 53.57% had motor delay, all of which was significantly different from the development of the HEU group for all domains (p<0.001). In addition to using the BSID-III, the majority of mothers were able to correctly indicate whether their child was developing at the same, or at a slower rate of development than children of the same age. This study demonstrates that infants who are HIV-exposed and infected are at risk of developmental delay.

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“…Our interpretation of the sequela in this child was as follows: hemiparesis and neurodevelopment delay appeared to be consequences of progressive encephalopathy due to HIV [9] and may have been propitiated by the introduction of antiretrovirals only at age six months. Strabismus and visual impairment were compatible with ocular lesions due to Toxoplasma, despite specific treatment instituted in the first days of life and maintained during a year.…”

Section: Discussionmentioning

confidence: 99%

Vertical transmission of HIV and toxoplasma by reactivation in a chronically infected woman

Fernandes

Vasconcellos

Araújo³

et al. 2009

Braz J Infect Dis

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Prevention of mother-to-child transmission of HIV and Toxoplasma dual infections in the immunocompromised patient remains a healthcare challenge. We report a case of congenital toxoplasmosis resulting from reactivation of latent infection in a severely immunodepressed HIV-infected pregnant woman, who had poor adherence to therapy; this case illustrates the difficulties encountered in management of such a rare condition.

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Neurologic and neurodevelopmental manifestations of pediatric HIV/AIDS: A global perspective

Cited by 151 publications

References 108 publications

Neurobehavioral Performance in Feline Immunodeficiency Virus Infection: Integrated Analysis of Viral Burden, Neuroinflammation, and Neuronal Injury in Cortex

Neurobehavioral Performance in Feline Immunodeficiency Virus Infection: Integrated Analysis of Viral Burden, Neuroinflammation, and Neuronal Injury in Cortex

Developmental delay in HIV-exposed infants in Harare, Zimbabwe

Vertical transmission of HIV and toxoplasma by reactivation in a chronically infected woman

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