Vih Juan Guillermo

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INIMUNOLOGA Y PATOGENESIS

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Andrew J. McMichael & Sarah L. Rowland-Jones. Cellular immune responses to HIV. 2001

The early CTL response to HIV

The viraemia rose to a peak (red line) and was followed by the CD8+ T-cell response to the

immunodominant Gag 263272 epitope presented by HLA-B27, demonstrated by the HLA-B27

epitope tetramer (mauve line).


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T cells either eliminate the virus or suppress it indefinitely as a harmless.

HIV undermines this control by infecting key immune cells, thereby

impairing the response of both the infected CD4+ T cells and the uninfectedCD8+ T cells.

Facilitates the escape of virus from immune control and the

collapse of the whole immune system.

HLA types associated with slow progression of the infection,

such as HLA-B27 and HLA-B57.

Confer increased susceptibility, such as HLA-B35

Kaslow, R. A. et al. Influence of combinations of human major histocompatibilitycomplex genes on the course of HIV-1 infection. Nature Med. 2, 405411 (1996).


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homozygosity at the HLA class I loci, which is also associated with morerapid progression of HIV, offers less opportunity for a diverse T-cellresponse.

Perforin is a protein, made by CD8+ T cells, that is present in granules, and

together with the granzymes is important in triggering target-cell death.

Interferon-g (IFN-g): Inhibits HIV replication.

Tumour-necrosis factor-a (TNF-a): Upregulate viral replication (activation

of the HIV promoter in the virus long terminal repeat (LTR).


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Expansion of HIV-specific CD8+ T cells inacute and chronic infection.


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CD4+ T-cell dependence of CD8+ T cells.


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Schematic representation of the relationship between virus replication rate,manifested as virus load, the level of CTL response and the selective pressure on

epitope escape mutants


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T CD4+ se utilizan para definir el estadio inmunolgico y para

recomendar el momento preciso para el inicio y monitoreo de la terapia

antirretroviral especfica.

Produccin diaria de ms de 1.000 millones de viriones


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Macrophage- and T-cell-specific steps in HIV-1 infection.

Las cepas M-trpicas son las que infectan macrfagos y linfocitos T primarios. No inducden formacion

de sincitios


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Formacin de sincicios celulares producido por el HIV-1 sobre la lnea celular MT-2.

Observacin al microscopio ptico invertido con un aumento de 16X


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co-receptores de entrada para el virus, menor eficiencia. Entre ellos se

encuentran el CCR2, CCR3, CCR8, CCR9, CX3CR1, y varios receptores

hurfanos como el STRL 33 ("Bonzo"), Gpr15 ("Bob"), Gpr1, APJ


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Delecin de 32 pb en la regin codificante del gen del CCR5 (CCR5-D32)

poblaciones caucsicas con 1% de homocigotas, y 10-20%

heterocigotas

heterocigotas CCR5+/D32 se encuentran con ms frecuencia en

cohortes de pacientes LTNP


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