Chemokine receptors get more and more interesting and confusing.

He et al. show that CCR3 and CCR5 can be used as receptors to infect
microglia.

Ditmar et al. summarize the confusion by stating "We show here that it
is oversimplistic to assume that chemokine co-receptor use accurately
reflects the cellular tropism of the virus."

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J He, Y Chen, M Farzan, H Choe, A Ohagen, S Gartner, J Busciglio, X
Yang, W Hofmann, W Newman, C R Mackay, J Sodroski & D Gabuzda.
CCR3 and CCR5 are co-receptors for HIV-1 infection of microglia (Letter
to Nature of 2/13/97). Nature 385, 645 (1997).

Abstract: Several members of the chemokine receptor family are used
together with CD4 for HIV-1 entry into target cells. T cell line-tropic
(T-tropic) HIV-1 viruses use the chemokine receptor CXCR4 as a
co-receptor, whereas macrophage-tropic (M-tropic) primary viruses use
CCR5. Individuals with defective CCR5 alleles exhibit resistance to
HIV-1 infection, suggesting that CCR5 has an important role in vivo in
HIV-1 replication. A subset of primary viruses can use CCR3 as well as
CCR5 as a co-receptor, but the in vivo contribution of CCR3 to HIV-1
infection and pathogenesis is unknown. HIV-1 infects the central nervous
system (CNS) and causes the dementia associated with AIDS. Here the
authors report that the major target cells for HIV-1 infection in the
CNS, the microglia, express both CCR3 and CCR5. The CCR3 ligand,
eotaxin, and an anti-CCR3 antibody inhibited HIV-1 infection of
microglia, as did MIP-1beta, which is a CCR5 ligand. Their results
suggest that both CCR3 and CCR5 promote efficient infection of the CNS
by HIV-1.

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Dittmar MT, McKnight A, Simmons G, Clapham PR, Weiss RA, Simmonds P.
HIV-1 tropism and co-receptor use. (Scientific Correspondence
to Nature dated 2/7/97). Nature 385, 495 (1997).

Chemoattractant cytokines (chemokines) act during inflammation by
binding to and signalling through 7-transmembrane cell-surface
receptors. There has been much excitement over the discovery that
certain chemokine receptors, in cooperation with CD4 molecules on the
T-cell surface, also serve as entry portals for HIV. Various isolates of
HIV-1 use different chemokine co-receptors. This helps to explain why
some HIV isolates preferentially infect one or other cell type, a
property known as HIV tropism. Although almost all HIV isolates can
infect T-helper lymphocytes that have been activated to proliferate in
primary culture, only certain isolates can also infect macrophages,
whereas others infect immortalized T-cell lines. We show here that it is
oversimplistic to assume that chemokine co-receptor use accurately
reflects the cellular tropism of the virus.

. . .

It also apparent that macrophages express CXCR4, yet are not infected
by T-cell-line-adapted strains of HIV-1. We conclude that the ability
of a virus to use a co-receptor molecule does not necessarily confer
on that virus the ability to use that molecule on all cell types.
Post-translation modifications of co-receptors on macrophages may affect
their availability for infection by some HIV-1 strains but not others.

. . .

We have shown that the selective pressure on HIV-1 to immune escape from
neutralization can result in gaining the use of co-receptors.
Conversely, selection to use these new co-receptors, as the virus
colonizes various cell types in vivo during the progression to AIDS, may
result in escape from neutralizing antibodies.