Modulation of CD4 lateral interaction with lymphocyte surface molecules induced by HIV-1 gp120

1995 ◽  
Vol 25 (5) ◽  
pp. 1306-1311 ◽  
Author(s):  
Umberto Dianzani ◽  
Manuela Bragardo ◽  
Donatella Buonfiglio ◽  
Valter Redoglia ◽  
Ada Funaro ◽  
...  
Keyword(s):  
Lateral Interaction ◽  
Surface Molecules ◽  
Lymphocyte Surface ◽  
Hiv 1

Membrane insertion of lymphocyte surface molecules

1980 ◽  
Vol 17 (12) ◽  
pp. 1575-1583 ◽  
Author(s):  
Charles L. Sidman ◽  
Tuvia Bercovici ◽  
Carlos Gitler
Keyword(s):  
Membrane Insertion ◽  
Surface Molecules ◽  
Lymphocyte Surface

scholarly journals Two distinct mechanisms for redistribution of lymphocyte surface macromolecules. II. Contrasting effects of local anesthetics and a calcium ionophore.

1978 ◽  
Vol 79 (2) ◽  
pp. 419-426 ◽  
Author(s):  
J Braun ◽  
K Fujiwara ◽  
T D Pollard ◽  
E R Unanue
Keyword(s):  
Local Anesthetic ◽  
Local Anesthetics ◽  
Calcium Ionophore ◽  
Contractile Proteins ◽  
Fc Receptor ◽  
Ionophore A23187 ◽  
Surface Complexes ◽  
Surface Molecules ◽  
Lymphocyte Surface ◽  
Dependent Link

In the previous study, lymphocyte surface molecules were separated into two subsets depending on whether capping was associated was associated with redistribution of cytoplasmic myosin. In the present study, the effects of the local anesthetic chlorpromazine and of the Ca2+ ionophore A23187 were compared. Both drugs affected the surface redistribution of immunoglobulin (Ig), Fc receptors, and the TL antigen--molecules that appear to cap by association with microfilaments--but had no effect on the Thy.1 (theta) and H2 antigens--molecules that cap slowly, apparently unlinked to microfilament function. The capping of Ig, Fc receptor, and TL was inhibited while that of H2 and theta was not. Both drugs reversed the Ig Fc receptor, and TL caps but not the H2 and theta caps. In the former group, the reversal of caps was accompanied by a parallel reversal of the myosin segregated to the cap area. The appearance of myosin after drug treatment varied: chlorpromazine resulted in a diffuse pattern similar to that of normal lymphocytes, whereas A23187 produced an array of aggregates and coarse filaments. The results are compatible with the view that two mechanisms for capping exist in the lymphocyte. The Ca2+ ionophore may affect capping of microfilament-dependent caps by producing a systemic activation of contractile proteins while chlorpromazine may act by disrupting a Ca2+-dependent link between surface complexes and the contractile proteins.

Characterization of the parasite-host cell interactions involved inTheileria parvasporozoite invasion of bovine lymphocytes

Parasitology ◽  
1996 ◽  
Vol 113 (3) ◽  
pp. 267-277 ◽  
Author(s):  
M. K. Shaw
Keyword(s):  
Host Cell ◽  
De Novo ◽  
Experimental Conditions ◽  
Surface Molecules ◽  
Lymphocyte Surface ◽  
Host Cell Interactions ◽  
Host Cell Surface ◽  
Ph Dependent ◽  
Bovine Lymphocytes

SUMMARYSporozoite invasion of bovine lymphocytes byTheileria parvais a pH-dependent process that occurs without the need forde novoprotein synthesis. The process was inhibited by RGD(S) peptides, fibronectin and, in the presence of serum, by antibodies reactive with fibronectin. Invasion was also blocked by a range of sulphated glycoconjugates, but treatment of lymphocytes with heparitinase did not inhibit entry. Enzymic modifications of the lymphocyte surface demonstrated that trypsin-insensitive glycoproteins containingO- andN-linked carbohydrates as well as phospholipase-sensitive molecules on the host cell surface were critical to sporozoite entry. Modification of the lymphocyte surface with NEM and DTT had only marginal effects on sporozoite binding but blocked parasite internalization. Invasion was also blocked by several antibodies which cross-reacted with sporozoite surface molecules. While only a few experimental conditions specifically blocked sporozoite binding, a wider range of reagents and treatments inhibited parasite entry. The reasons for this are discussed in terms of the nature of the zippering process that facilitates sporozoite internalization.

Cell adhesion through αV-containing integrins is required for efficient HIV-1 infection in macrophages

Blood ◽  
2009 ◽  
Vol 113 (6) ◽  
pp. 1278-1286 ◽  
Author(s):  
Ester Ballana ◽  
Eduardo Pauls ◽  
Jordi Senserrich ◽  
Bonaventura Clotet ◽  
Françoise Perron-Sierra ◽  
...  
Keyword(s):  
Cell Attachment ◽  
Signal Transduction Pathway ◽  
Nuclear Factor Κb ◽  
Susceptibility To Infection ◽  
Surface Molecules ◽  
Immunodeficiency Virus ◽  
Mitogen Activated Protein ◽  
Monocytes And Macrophages ◽  
Hiv 1

AbstractMonocytes and macrophages are an important reservoir of human immunodeficiency virus (HIV) and may represent the largest reservoir of this virus in tissues. Differentiation of monocytes into macrophages leads to cell attachment and susceptibility to infection and replication of HIV. Among other cell-surface molecules, integrins are overexpressed during monocyte-macrophage differentiation and may play a role in the replication cycle of envelope viruses including HIV. Here, we show that inhibition of αV integrin in monocyte-derived macrophages, by RNA interference or their inhibition by a selective small heterocyclic RGD-mimetic nonpeptide compound, inhibited the replication of HIV in the absence of cytotoxicity. Interference or inhibition of αV integrins triggered a signal transduction pathway, leading to down-regulation of nuclear factor-κB–dependent HIV-1 transcription. Such inhibition was mediated by a MAP-kinase signaling cascade, probably involving ERK1/2, p38-mitogen–activated protein kinases, and HSP27. In conclusion, our results reveal a significant role of integrin αV-mediated adhesion in HIV-1 infection of macrophages.

Modulation of cell surface molecules during HIV-1 infection of H9 cells. An immunoelectron microscopic study

AIDS ◽  
1992 ◽  
Vol 6 (10) ◽  
pp. 1105-1116 ◽  
Author(s):  
Timo Meerloo ◽  
Henk K. Parmentier ◽  
Albert D.M.E. Osterhaus ◽  
Jaap Goudsmit ◽  
Henk-Jan Schuurman
Keyword(s):  
Cell Surface ◽  
Microscopic Study ◽  
Cell Surface Molecules ◽  
Surface Molecules ◽  
Hiv 1

Is CD4 sufficient for HIV entry? Cell surface molecules involved in HIV infection

1993 ◽  
Vol 342 (1299) ◽  
pp. 67-73 ◽  
Keyword(s):  
Cell Adhesion ◽  
Cell Surface ◽  
Cell Adhesion Molecules ◽  
Virus Entry ◽  
Neural Cells ◽  
Cell Surface Molecules ◽  
Virus Envelope ◽  
Surface Molecules ◽  
Hiv Entry ◽  
Hiv 1

HIV-1, HIV-2 and SIV each bind to CD4 as the first step in virus entry. However, alternative receptors may also be used. HIV-1 binds to glycolipids with terminal galactosylceramide residues on neural cells; opsonized virus binds to Fc receptors; HIV-2 can infect certain CD4-negative cells. Further receptors may also play a role in CD4-mediated infection, including cell adhesion molecules and possibly cell surface proteinases. After binding to CD4, immunodeficiency viruses require secondary molecules to effect fusion between the virus envelope and the cell membrane; these accessory requirements differ between HIV-1, HIV-2 and SIV.

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