scholarly journals Oligomerization of the Macrophage Mannose Receptor Enhances gp120-mediated Binding of HIV-1

2009 ◽  
Vol 284 (17) ◽  
pp. 11027-11038 ◽  
Author(s):  
Joey Lai ◽  
Oliver K. Bernhard ◽  
Stuart G. Turville ◽  
Andrew N. Harman ◽  
John Wilkinson ◽  
...  
Keyword(s):  
Mannose Receptor ◽  
Macrophage Mannose Receptor ◽  
Hiv 1

scholarly journals Mannose receptor is an HIV restriction factor counteracted by Vpr in macrophages

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jay Lubow ◽  
Maria C Virgilio ◽  
Madeline Merlino ◽  
David R Collins ◽  
Michael Mashiba ◽  
...  
Keyword(s):  
Biosynthetic Pathway ◽  
Human Monocyte ◽  
Mannose Receptor ◽  
Evolutionary Conservation ◽  
Restriction Factor ◽  
Free Virus ◽  
Response System ◽  
Macrophage Mannose Receptor ◽  
Specific Restriction ◽  
Hiv 1

HIV-1 Vpr is necessary for maximal HIV infection and spread in macrophages. Evolutionary conservation of Vpr suggests an important yet poorly understood role for macrophages in HIV pathogenesis. Vpr counteracts a previously unknown macrophage-specific restriction factor that targets and reduces the expression of HIV Env. Here, we report that the macrophage mannose receptor (MR), is a restriction factor targeting Env in primary human monocyte-derived macrophages. Vpr acts synergistically with HIV Nef to target distinct stages of the MR biosynthetic pathway and dramatically reduce MR expression. Silencing MR or deleting mannose residues on Env rescues Env expression in HIV-1-infected macrophages lacking Vpr. However, we also show that disrupting interactions between Env and MR reduces initial infection of macrophages by cell-free virus. Together these results reveal a Vpr-Nef-Env axis that hijacks a host mannose-MR response system to facilitate infection while evading MR’s normal role, which is to trap and destroy mannose-expressing pathogens.

scholarly journals Mannose receptor is a restriction factor of HIV in macrophages and is counteracted by the accessory protein Vpr

2019 ◽  
Author(s):  
Jay Lubow ◽  
David R. Collins ◽  
Mike Mashiba ◽  
Brian Peterson ◽  
Maria Virgilio ◽  
...  
Keyword(s):  
Biosynthetic Pathway ◽  
Human Monocyte ◽  
Mannose Receptor ◽  
Evolutionary Conservation ◽  
Restriction Factor ◽  
Free Virus ◽  
Response System ◽  
Macrophage Mannose Receptor ◽  
Specific Restriction ◽  
Hiv 1

AbstractHIV-1 Vpr is necessary to support HIV infection and spread in macrophages. Evolutionary conservation of Vpr suggests an important yet poorly understood role for macrophages in HIV pathogenesis. Vpr counteracts a previously unknown macrophage-specific restriction factor that targets and reduces the expression of HIV Env. Here, we report that the macrophage mannose receptor (MR), is the restriction factor targeting Env in primary human monocyte-derived macrophages. Vpr acts synergistically with HIV Nef to target distinct stages of the MR biosynthetic pathway and dramatically reduce MR expression. Silencing MR or deleting mannose residues on Env rescues Env expression in HIV-1-infected macrophages lacking Vpr. However, we also show that disrupting interactions between Env and MR reduces initial infection of macrophages by cell-free virus. Together these results reveal a Vpr-Nef-Env axis that hijacks a macrophage mannose-MR response system to facilitate infection while evading MR’s normal role, which is to trap and destroy mannose-expressing pathogens.

HIV Impairs Alveolar Macrophage Mannose Receptor Function Against Pneumocystis carinii

CHEST Journal ◽  
1993 ◽  
Vol 103 (2) ◽  
pp. 111S-112S ◽  
Author(s):  
Henry Koziel ◽  
B.A. Kruskal ◽  
R.A.B Ezekowitz ◽  
R.M Rose
Keyword(s):  
Alveolar Macrophage ◽  
Pneumocystis Carinii ◽  
Mannose Receptor ◽  
Receptor Function ◽  
Macrophage Mannose Receptor

Dexamethasone Blocks the Interferon-γ-Mediated Downregulation of the Macrophage Mannose Receptor

1994 ◽  
Vol 312 (2) ◽  
pp. 367-374 ◽  
Author(s):  
V.L. Shepherd ◽  
H.B. Cowan ◽  
R. Abdolrasulnia ◽  
S. Vick
Keyword(s):  
Mannose Receptor ◽  
Interferon Γ ◽  
Macrophage Mannose Receptor

scholarly journals Absence of the Macrophage Mannose Receptor in Mice Does Not Increase Susceptibility to Pneumocystis carinii Infection In Vivo

2003 ◽  
Vol 71 (11) ◽  
pp. 6213-6221 ◽  
Author(s):  
Steve D. Swain ◽  
Sena J. Lee ◽  
Michel C. Nussenzweig ◽  
Allen G. Harmsen
Keyword(s):  
Pneumocystis Carinii ◽  
Hydrolytic Enzymes ◽  
Mannose Receptor ◽  
Opportunistic Pathogen ◽  
Cell Types ◽  
Surface Expression ◽  
Wild Type ◽  
Macrophage Mannose Receptor

ABSTRACT Host defense against the opportunistic pathogen Pneumocystis carinii requires functional interactions of many cell types. Alveolar macrophages are presumed to be a vital host cell in the clearance of P. carinii, and the mechanisms of this interaction have come under scrutiny. The macrophage mannose receptor is believed to play an important role as a receptor involved in the binding and phagocytosis of P. carinii. Although there is in vitro evidence for this interaction, the in vivo role of this receptor in P. carinii clearance in unclear. Using a mouse model in which the mannose receptor has been deleted, we found that the absence of this receptor is not sufficient to allow infection by P. carinii in otherwise immunocompetent mice. Furthermore, when mice were rendered susceptible to P. carinii by CD4+ depletion, mannose receptor knockout mice (MR-KO) had pathogen loads equal to those of wild-type mice. However, the MR-KO mice exhibited a greater influx of phagocytes into the alveoli during infection. This was accompanied by increased pulmonary pathology in the MR-KO mice, as well as greater accumulation of glycoproteins in the alveoli (glycoproteins, including harmful hydrolytic enzymes, are normally cleared by the mannose receptor). We also found that the surface expression of the mannose receptor is not downregulated during P. carinii infection in wild-type mice. Our findings suggest that while the macrophage mannose receptor may be important in the recognition of P. carinii, in vivo, this mechanism may be redundant, and the absence of this receptor may be compensated for.

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