Induction of interleukin-1 and glucocorticoid hormones by HIV promotes viral replication and links human chromosome 2 to AIDS pathogenesis: genetic mechanisms and therapeutic implications.

Abstract:

:Human immunodeficiency virus may regulate its replication by stimulating the synthesis of interleukin-1. Interleukin-1, in turn, has the ability to stimulate the human immunodeficiency virus enhancer region. The human genes responsible for interleukin-1 and interleukin-1 receptor antagonist synthesis are located on the long arm of chromosome 2. Coincidentally, the trans-activation responsive ribonucleic acid element in the R region of the long terminal repeat of human immunodeficiency virus-1 has been found to interact directly with a factor present on the long arm of chromosome 2 to facilitate transactivation by the human immunodeficiency virus Tat protein. The human CD26 gene is also located on the long arm of chromosome 2. CD26 is a lymphocyte cell surface antigen that is stimulated by interleukin-1 and serves with CD4 as a coreceptor that interacts with the V3 loop in gp120 of human immunodeficiency virus. The human immunodeficiency virus-induced interleukin-1 excess, thus, serves human immunodeficiency virus by enhancing replication, and by increasing human immunodeficiency virus infectivity via activation of CD26. IL-1 also adversely affects acquired immune deficiency syndrome-related Kaposi's sarcoma. Several genetic treatments for human immunodeficiency virus infection are proposed.

journal_name

Med Hypotheses

journal_title

Medical hypotheses

authors

Corley PA

doi

10.1016/s0306-9877(97)90040-2

subject

Has Abstract

pub_date

1997-05-01 00:00:00

pages

415-21

issue

5

eissn

0306-9877

issn

1532-2777

pii

S0306-9877(97)90040-2

journal_volume

48

pub_type

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