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J Virol, February 1998, p. 1334-1344, Vol. 72, No. 2
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Differential Tropism and Chemokine Receptor Expression of Human Immunodeficiency Virus Type 1 in Neonatal Monocytes, Monocyte-Derived Macrophages, and Placental Macrophages

Warwick R. Fear,1 Alison M. Kesson,2 Hassan Naif,1 Garry W. Lynch,1 and Anthony L. Cunningham1,*

Centre for Virus Research, Westmead Institutes of Health Research and Australian National Centre for HIV Virology Research, Westmead Hospital, The University of Sydney, Sydney,1 and Discipline of Pathology, Faculty of Medicine and Health Sciences and Department of Microbiology and Infectious Diseases, Hunter Area Pathology Service, John Hunter Hospital, Newcastle,2 Australia

Received 30 June 1997/Accepted 29 September 1997

Laboratory-adapted (LA) macrophage-tropic (M-tropic) human immunodeficiency virus type 1 (HIV-1) isolates (e.g., HIV-1Ba-L) and low-passage primary (PR) isolates differed markedly in tropism for syngeneic neonatal monocytes, monocyte-derived macrophages (MDMs), and placental macrophages (PMs). Newly adherent neonatal monocytes and cultured PMs were highly refractory to infection with PR HIV-1 isolates yet were permissive for LA M-tropic isolates. Day 4 MDMs were also permissive for LA M-tropic isolates and additionally, were permissive for over half the PR isolates tested. Qualitative differences in PR HIV-1 infection of monocytes/MDMs could not be correlated with CD4 levels alone, and in all three cell types the block to PR HIV-1 strain replication preceded reverse transcription. Neonatal monocyte susceptibility to PR HIV-1 strains correlated with increasing CCR-5 expression during maturation. CCR-5 could not be detected on newly adherent (day 1) neonatal monocytes, in contrast to adult monocytes (H. Naif et al., J. Virol. 72:830-836, 1998), but was readily detectable after 4 to 7 days of culture. However, moderate CCR-5 mRNA levels were present in day 1 neonatal monocytes and remained constant during monocyte maturation. CCR-5 was not detectable on the surface of PMs, yet the receptor was present within permeabilized cells. Notably, two brain-derived PR HIV-1 isolates from a single patient, differing in their V3 loops, were discordant in their abilities to infect neonatal monocytes/MDMs and PMs, yet both isolates could infect newly adherent adult monocytes. Together these data strongly suggest that LA HIV-1 isolates are able to infect neonatal monocytes at earlier stages of maturation and lower-level expression of CCR-5 than PR isolates. The differences between neonatal and adult monocytes in susceptibility to PR isolates may also be related to the level of CCR-5 expression.

* Corresponding author. Mailing address: Room 2145, Level 2, Centre for Virus Research, Westmead Institutes of Health Research, Westmead Hospital, The University of Sydney, Westmead NSW 2145, Australia. Phone: 61 2 9845 6344. Fax: 61 2 9845 8300. E-mail: tonyc{at}westmed.wh.su.edu.au.




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