Learning impairment following intracerebral administration of the HIV envelope protein gp120 or a VIP antagonist

@article{Glowa1992LearningIF,
  title={Learning impairment following intracerebral administration of the HIV envelope protein gp120 or a VIP antagonist},
  author={John R. Glowa and Leigh V. Panlilio and Douglas E Brenneman and Illana Gozes and Mati Fridkin and Joannam . Hill},
  journal={Brain Research},
  year={1992},
  volume={570},
  pages={49-53}
}

Central nervous system damage produced by expression of the HIV-1 coat protein gpl20 in transgenic mice

TLDR
In vivo evidence is provided that gp120 plays a key part in HIV-1-associated nervous system impairment and this model should facilitate the evaluation and development of therapeutic strategies aimed at HIV–brain interactions.

HIV- and FIV-Derived gp120 Alter Spatial Memory, LTP, and Sleep in Rats

TLDR
The results suggest that HIVgp120 causes neurophysiological abnormalities and therefore may facilitate HAD development in AIDS patients.

Exploitation of the HIV‐1 coat glycoprotein, gp120, in neurodegenerative studies in vivo

TLDR
It has been shown that brain neocortical cell death is caused in rat by intracerebroventricular injection of a recombinant gp120 coat protein, and that this occurs via apoptosis, which broadens knowledge in the pathophysiology of the reported neuronal cell loss.

Mechanisms of HIV type 1-induced cognitive impairment: evidence for hippocampal cholinergic involvement with overstimulation of the VIPergic system by the viral coat protein core.

TLDR
The predominant cognitive-impairing component of HIV-1 is its viral coat glycoproteins, gp120 impairs memory by overstimulating pathways that normally sustain memory, the cognitive effect of gp120 is mediated by its protein core, and gp120 likely impairsMemory by affecting the cholinergic/VIPergic system.
...

References

SHOWING 1-10 OF 30 REFERENCES

Neuronal cell killing by the envelope protein of HIV and its prevention by vasoactive intestinal peptide

TLDR
It is suggested that the neuronal deficits associated with HIV may not be entirely a result of infectivity, but that gp120 shed from HIV could directly produce the neuropathology as a consequence of its interference with endogenous neurotrophic substances.

Neuronal injury due to HIV‐1 envelope protein is blocked by anti‐gp120 antibodies but not by anti‐CD4 antibodies

TLDR
It is suggested that injury of central neurons engendered by gp120 may be responsible, at least in part, for the neurologic manifestations observed in as many as ± of the patients with acquired immunodeficiency syndrome, such as dementia, myelopathy, and visual loss, even in the absence of superinfection.

HIV-1 coat protein neurotoxicity prevented by calcium channel antagonists.

TLDR
Immunoprecipitation with antibody to gp120, but not with control immunoglobulin-containing serum, depleted solutions of the viral envelope protein and also prevented both the rise in intracellular calcium and neuronal toxicity, and treatment with calcium channel antagonists may prove useful in mitigating HIV-1-related neuronal injury.

Octapeptides deduced from the neuropeptide receptor-like pattern of antigen T4 in brain potently inhibit human immunodeficiency virus receptor binding and T-cell infectivity.

  • C. PertJ. Hill W. Farrar
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1986
The differentiation antigen T4, present on the helper/inducer subset of T lymphocytes, is thought to serve as the receptor for the human immunodeficiency virus (HIV). We find that a 60-kDa protein,

An antagonist to vasoactive intestinal peptide affects cellular functions in the central nervous system.

TLDR
A potent VIP antagonist is described which interacts with two functionally distinct VIP receptors in the central nervous system and appears to be a competitive blocker for both VIP-mediated increases in cAMP formation or VIP-associated maintenance of neuronal survival in spinal cord cultures.

Prospect for prevention of human immunodeficiency virus infection: purified 120-kDa envelope glycoprotein induces neutralizing antibody.

TLDR
The induction of neutralizing antibody indicates that a gp120 subunit vaccine against HIV is theoretically possible, and other retrovirus models have shown that purified external glycoprotein subunits are immunogenic.

The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex.

TLDR
Within the context of the permissive effect of immunosuppression, genetic changes in HIV-1 may underlie the neuropathological heterogeneity of the AIDS dementia complex and its relatively independent course in relation to the systemic manifestations of AIDS noted in some patients.

Autoradiographic localization of T4 antigen, the HIV receptor, in human brain.

TLDR
Using a novel autoradiographic technique and a monoclonal antibody to T4, the entry protein for the AIDS virus HIV, the distribution of T4 was determined in selected areas of the human brain, demonstrating a conservation of both the antigen and the antigen distribution.

Human immunodeficiency virus-infected macrophages produce soluble factors that cause histological and neurochemical alterations in cultured human brains.

TLDR
It is suggested that HIV-infected macrophages, infected both in vitro as well as derived from AIDS patients' peripheral blood, produce factors that cause reproducible histochemical, ultrastructural, and functional abnormalities in human brain aggregates.

Vasoactive intestinal peptide and electrical activity influence neuronal survival.

  • D. BrennemanL. Eiden
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1986
TLDR
Under conditions of electrical blockade a neurotrophic action of VIP on neuronal survival can be demonstrated, and two closely related peptides were found not to increase the number of neurons in TTX-treated cultures.