摘要:

The life cycle of HIV can be divided into two distinct stages: intracellular and extracellular. The prevailing view is that the intracellular stage provides the only locus for regulating the virus in response to physiologic stimuli. Such regulation is accomplished by modulating the rates of transcription, translation and viral assembly. The extracellular stage consists of physical processes such as diffusion, adhesion and penetration of cells by viral particles. These latter processes are commonly thought to be“automatic”and not subject to regulation. For the past several years, we have developed means of more carefully measuring and characterizing the extracellular stage of HIV infection, and we have obtained evidence indicating that novel regulatory processes do, in fact, take place during this extracellular stage. We believe that this extracellular regulation permits HIV to adapt to a wide range of physiologic cell densities, to maintain persistent but slow growing infection, and to defeat the protective activity of humoral blockers. The overall purpose of this review is to consider our evidence for this hypothesis.

ISSN:0883-0185    

DOI:10.3109/08830189209056638

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0883-0185    

DOI:10.3109/08830189209056639

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Components of the host immune response that constrain virus replication and affect long-lasting antiviral immunity following HIV infection are incompletely defined. IFNs are critical participants in host antiviral processes. While IFN induces significant anti-retroviral activities, they also serve as harbingers for poor clinical outcomes. Moreover, monocytes, a major cellular source of IFN and HIV in man, are poor producer cells for IFN following HIV infection. Indeed, HIV infection of monocytes results in a diminished production and induction of IFN. IFN is only produced during cell to cell contact between HIV-infected cells and uninfected PBMC. Analysis of the biologic activity of HIV-induced IFN(s) shows that it poorly restricts HIV replication. Thus, the role of IFN in HIV disease is complex and seemingly paradoxical. The diminished capacity of HIV-infected monocytes to produce IFN and the production of defective IFNs likely reflect specific viral adaptive mechanisms for persistent infection.

ISSN:0883-0185    

DOI:10.3109/08830189209056640

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Simian immunodeficiency virus (SIV) infection of macaques is the best available animal model for studying the pathogenesis of AIDS. Experimental inoculation of macaques with SIV results in a persistent infection that leads to immunodeficiency, opportunistic infections, and death. Most aspects of the illness, including immunologic and virologic parameters, are easily quantified. Furthermore, pathologic processes can be evaluated throughout the course of experimental infection. Recently, molecular clones of SIV proviral DNA have been used to study genetic variation and specific viral determinants of pathogenesis. Considered together, these observations support the continued detailed study of SIV infection of macaques as a model for human AIDS.

ISSN:0883-0185    

DOI:10.3109/08830189209056641

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

An attempt is made to summarize the evidence that humoral immune responses in natural HIV-1 infection play a role in clearance of the initial burst of replication as well as in protection against rapid disease progression. Therefore, the so-called“asymptomatic carrier state”was defined on the basis of immunological characteristics, such as CD4+ cell number, CD45RA-CD29+ cell number, CD4+ proliferative responses to anti-CD3 mAbs and soluble activation markers, as well as virological characteristics such as the state of the viral genome in the cell, levels of genomic RNA production, antigenemia, viremia and virus phenotype. During natural infection two major classes HIV-1 neutralizing and cell-fusion inhibiting antibodies are elicited. One population directed against mostly continuous epitopes localized in the third variable domain (V3) of the envelope and one against discontinuous epitopes of the envelope. The last population blocks gp120-CD4 attachment, the first does not. The role of each of these populations of functional antibodies, in the clearance of viremia and the maintenance of the asymptomatic carrier state is discussed.

ISSN:0883-0185    

DOI:10.3109/08830189209056642

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0883-0185    

DOI:10.3109/08830189209056637

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor