Dendritic-cell interactions with HIV: infection and viral dissemination
Key Points Dendritic cells (DCs) are located in the mucosae and the lymphoid tissues. They are proposed to be among the first cells to encounter HIV during sexual transmission. The main populations of DCs include myeloid DCs and plasmacytoid DCs in the blood, and Langerhans cells in the tissues. Mye...
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description | Key Points
Dendritic cells (DCs) are located in the mucosae and the lymphoid tissues. They are proposed to be among the first cells to encounter HIV during sexual transmission.
The main populations of DCs include myeloid DCs and plasmacytoid DCs in the blood, and Langerhans cells in the tissues. Myeloid DCs, plasmacytoid DCs and Langerhans cells are all susceptible to infection with HIV; they can also transfer HIV to CD4
+
T cells.
Follicular DCs can trap and maintain large quantities of HIV, thereby functioning as a persistent reservoir of virus.
Immunomodulation of DCs by HIV infection is a key aspect of viral pathogenesis, particularly through the modulation or interference of the antigen-presenting function of DCs.
DCs express high levels of C-type lectins, including DC-specific intercellular adhesion molecule 3 (ICAM3)-grabbing non-integrin (DC-SIGN; also known as CD209). C-type lectins are the main HIV attachment factors at the surface of dermal and mucosal DCs.
DCs have DC-SIGN-dependent and DC-SIGN-independent mechanisms of HIV
trans
-infection of CD4
+
T cells. The efficiency of HIV transmission can be increased by maturation of DCs.
The transfer of virus from DCs to CD4
+
T cells occurs in three discrete steps. First, DCs capture and bind HIV. Second, HIV traffics within these DCs. And third, HIV is transferred to CD4
+
T cells by a process that is known as
trans
-infection.
DC-mediated HIV
trans
-infection might occur by several distinct processes that can take place concurrently, including rapid HIV
trans
-infection through infectious synapses and exosome-associated viruses. HIV transmission can also be mediated by
de novo
viral production in DCs, known as
cis
-infection.
Elucidating the interactions of HIV with DCs will be vital to uncover the contribution of DCs to viral pathogenesis.
HIV has evolved ways to exploit dendritic cells to facilitate spread of the virus through the body. Dendritic cells can mediate the transfer of HIV to target CD4
+
T cells through several distinct mechanisms, as discussed in this Review.
Dendritic cells (DCs) are crucial for the generation and the regulation of adaptive immunity. Because DCs have a pivotal role in marshalling immune responses, HIV has evolved ways to exploit DCs, thereby facilitating viral dissemination and allowing evasion of antiviral immunity. Defining the mechanisms that underlie cell–cell transmission of HIV and understanding the role of DCs in this process should help us in the fight again |
doi_str_mv | 10.1038/nri1960 |
format | Article |
fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1796806</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A179279114</galeid><sourcerecordid>A179279114</sourcerecordid><originalsourceid>FETCH-LOGICAL-c612t-d00e71f678bd4ec1e64003ccb90fe490b71772b35dea627bfe656efc7dda731e3</originalsourceid><addsrcrecordid>eNqFkm9rFDEQxoNYbD3FT6AsFVp9sTXZ3Sa7vhBK1fagIPjvbcgms3cpe0lNslW_vXPd89pVQfIiYeaXh5lnhpAnjB4xWtavXLCs4fQe2WOVqHImKnZ_-y7LXfIwxktKGcfMA7LLBOUlq_keOXsLzgSbrM419H1mXYKgdLLexey7TcvsfP71NYY7uAlmypns2gbVZ8bGCCvr1Dr-iOx0qo_weHPPyJf37z6fnucXH87mpycXueasSLmhFATruKhbU4FmwCtKS63bhnZQNbQVTIiiLY8NKF6ItgN-zKHTwhglSgbljLwZda-GdgVGg0tYi7wKdqXCT-mVldOMs0u58NeSiYbX2PWMHGwEgv82QExyZeO6deXAD1Hyuqlr3vwfLGhV1KPi_h_gpR-CQxdkUVRoOVqN0PMRWqgeJNrpsTq9VpQnWFohGsYqpI7-QeExaLT2DjqL8cmHl5MPyCT4kRZqiFHOP32csgd32CWoPi2j74ebWU_BwxHUwccYoNvay6hcr5vcrBuSz-5O45bb7BcCL0YgYsotINx687fW0xHFhRoCbLV-538By1Tlgg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>224161631</pqid></control><display><type>article</type><title>Dendritic-cell interactions with HIV: infection and viral dissemination</title><source>MEDLINE</source><source>Nature</source><source>Wiley Online Library Free Content</source><source>Access via Wiley Online Library</source><source>IngentaConnect Free/Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Wu, Li ; KewalRamani, Vineet N</creator><creatorcontrib>Wu, Li ; KewalRamani, Vineet N</creatorcontrib><description>Key Points
Dendritic cells (DCs) are located in the mucosae and the lymphoid tissues. They are proposed to be among the first cells to encounter HIV during sexual transmission.
The main populations of DCs include myeloid DCs and plasmacytoid DCs in the blood, and Langerhans cells in the tissues. Myeloid DCs, plasmacytoid DCs and Langerhans cells are all susceptible to infection with HIV; they can also transfer HIV to CD4
+
T cells.
Follicular DCs can trap and maintain large quantities of HIV, thereby functioning as a persistent reservoir of virus.
Immunomodulation of DCs by HIV infection is a key aspect of viral pathogenesis, particularly through the modulation or interference of the antigen-presenting function of DCs.
DCs express high levels of C-type lectins, including DC-specific intercellular adhesion molecule 3 (ICAM3)-grabbing non-integrin (DC-SIGN; also known as CD209). C-type lectins are the main HIV attachment factors at the surface of dermal and mucosal DCs.
DCs have DC-SIGN-dependent and DC-SIGN-independent mechanisms of HIV
trans
-infection of CD4
+
T cells. The efficiency of HIV transmission can be increased by maturation of DCs.
The transfer of virus from DCs to CD4
+
T cells occurs in three discrete steps. First, DCs capture and bind HIV. Second, HIV traffics within these DCs. And third, HIV is transferred to CD4
+
T cells by a process that is known as
trans
-infection.
DC-mediated HIV
trans
-infection might occur by several distinct processes that can take place concurrently, including rapid HIV
trans
-infection through infectious synapses and exosome-associated viruses. HIV transmission can also be mediated by
de novo
viral production in DCs, known as
cis
-infection.
Elucidating the interactions of HIV with DCs will be vital to uncover the contribution of DCs to viral pathogenesis.
HIV has evolved ways to exploit dendritic cells to facilitate spread of the virus through the body. Dendritic cells can mediate the transfer of HIV to target CD4
+
T cells through several distinct mechanisms, as discussed in this Review.
Dendritic cells (DCs) are crucial for the generation and the regulation of adaptive immunity. Because DCs have a pivotal role in marshalling immune responses, HIV has evolved ways to exploit DCs, thereby facilitating viral dissemination and allowing evasion of antiviral immunity. Defining the mechanisms that underlie cell–cell transmission of HIV and understanding the role of DCs in this process should help us in the fight against HIV infection. This Review highlights the latest advances in our understanding of the interactions between DCs and HIV, focusing on the mechanisms of DC-mediated viral dissemination.</description><identifier>ISSN: 1474-1733</identifier><identifier>EISSN: 1474-1741</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1038/nri1960</identifier><identifier>PMID: 17063186</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Antigens ; Biomedical and Life Sciences ; Biomedicine ; CD4-Positive T-Lymphocytes - immunology ; Cell Adhesion Molecules - immunology ; Chemokines ; Dendritic cells ; Dendritic Cells - immunology ; Disease transmission ; Drug resistance ; Health aspects ; HIV ; HIV (Viruses) ; HIV - immunology ; HIV Infections - immunology ; HIV Infections - transmission ; HIV Infections - virology ; Human immunodeficiency virus ; Humans ; Immune response ; Immunology ; Infections ; Lectins, C-Type - immunology ; Lymphocytes ; Pathogenesis ; Receptors, Cell Surface - immunology ; review-article ; Viral infections ; Virus Internalization</subject><ispartof>Nature Reviews: Immunology, 2006-11, Vol.6 (11), p.859-868</ispartof><rights>Springer Nature Limited 2006</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Nov 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c612t-d00e71f678bd4ec1e64003ccb90fe490b71772b35dea627bfe656efc7dda731e3</citedby><cites>FETCH-LOGICAL-c612t-d00e71f678bd4ec1e64003ccb90fe490b71772b35dea627bfe656efc7dda731e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,2727,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17063186$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Li</creatorcontrib><creatorcontrib>KewalRamani, Vineet N</creatorcontrib><title>Dendritic-cell interactions with HIV: infection and viral dissemination</title><title>Nature Reviews: Immunology</title><addtitle>Nat Rev Immunol</addtitle><addtitle>Nat Rev Immunol</addtitle><description>Key Points
Dendritic cells (DCs) are located in the mucosae and the lymphoid tissues. They are proposed to be among the first cells to encounter HIV during sexual transmission.
The main populations of DCs include myeloid DCs and plasmacytoid DCs in the blood, and Langerhans cells in the tissues. Myeloid DCs, plasmacytoid DCs and Langerhans cells are all susceptible to infection with HIV; they can also transfer HIV to CD4
+
T cells.
Follicular DCs can trap and maintain large quantities of HIV, thereby functioning as a persistent reservoir of virus.
Immunomodulation of DCs by HIV infection is a key aspect of viral pathogenesis, particularly through the modulation or interference of the antigen-presenting function of DCs.
DCs express high levels of C-type lectins, including DC-specific intercellular adhesion molecule 3 (ICAM3)-grabbing non-integrin (DC-SIGN; also known as CD209). C-type lectins are the main HIV attachment factors at the surface of dermal and mucosal DCs.
DCs have DC-SIGN-dependent and DC-SIGN-independent mechanisms of HIV
trans
-infection of CD4
+
T cells. The efficiency of HIV transmission can be increased by maturation of DCs.
The transfer of virus from DCs to CD4
+
T cells occurs in three discrete steps. First, DCs capture and bind HIV. Second, HIV traffics within these DCs. And third, HIV is transferred to CD4
+
T cells by a process that is known as
trans
-infection.
DC-mediated HIV
trans
-infection might occur by several distinct processes that can take place concurrently, including rapid HIV
trans
-infection through infectious synapses and exosome-associated viruses. HIV transmission can also be mediated by
de novo
viral production in DCs, known as
cis
-infection.
Elucidating the interactions of HIV with DCs will be vital to uncover the contribution of DCs to viral pathogenesis.
HIV has evolved ways to exploit dendritic cells to facilitate spread of the virus through the body. Dendritic cells can mediate the transfer of HIV to target CD4
+
T cells through several distinct mechanisms, as discussed in this Review.
Dendritic cells (DCs) are crucial for the generation and the regulation of adaptive immunity. Because DCs have a pivotal role in marshalling immune responses, HIV has evolved ways to exploit DCs, thereby facilitating viral dissemination and allowing evasion of antiviral immunity. Defining the mechanisms that underlie cell–cell transmission of HIV and understanding the role of DCs in this process should help us in the fight against HIV infection. This Review highlights the latest advances in our understanding of the interactions between DCs and HIV, focusing on the mechanisms of DC-mediated viral dissemination.</description><subject>Antigens</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Cell Adhesion Molecules - immunology</subject><subject>Chemokines</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Disease transmission</subject><subject>Drug resistance</subject><subject>Health aspects</subject><subject>HIV</subject><subject>HIV (Viruses)</subject><subject>HIV - immunology</subject><subject>HIV Infections - immunology</subject><subject>HIV Infections - transmission</subject><subject>HIV Infections - virology</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunology</subject><subject>Infections</subject><subject>Lectins, C-Type - immunology</subject><subject>Lymphocytes</subject><subject>Pathogenesis</subject><subject>Receptors, Cell Surface - immunology</subject><subject>review-article</subject><subject>Viral infections</subject><subject>Virus Internalization</subject><issn>1474-1733</issn><issn>1474-1741</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkm9rFDEQxoNYbD3FT6AsFVp9sTXZ3Sa7vhBK1fagIPjvbcgms3cpe0lNslW_vXPd89pVQfIiYeaXh5lnhpAnjB4xWtavXLCs4fQe2WOVqHImKnZ_-y7LXfIwxktKGcfMA7LLBOUlq_keOXsLzgSbrM419H1mXYKgdLLexey7TcvsfP71NYY7uAlmypns2gbVZ8bGCCvr1Dr-iOx0qo_weHPPyJf37z6fnucXH87mpycXueasSLmhFATruKhbU4FmwCtKS63bhnZQNbQVTIiiLY8NKF6ItgN-zKHTwhglSgbljLwZda-GdgVGg0tYi7wKdqXCT-mVldOMs0u58NeSiYbX2PWMHGwEgv82QExyZeO6deXAD1Hyuqlr3vwfLGhV1KPi_h_gpR-CQxdkUVRoOVqN0PMRWqgeJNrpsTq9VpQnWFohGsYqpI7-QeExaLT2DjqL8cmHl5MPyCT4kRZqiFHOP32csgd32CWoPi2j74ebWU_BwxHUwccYoNvay6hcr5vcrBuSz-5O45bb7BcCL0YgYsotINx687fW0xHFhRoCbLV-538By1Tlgg</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Wu, Li</creator><creator>KewalRamani, Vineet N</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7QR</scope><scope>7RV</scope><scope>7T5</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20061101</creationdate><title>Dendritic-cell interactions with HIV: infection and viral dissemination</title><author>Wu, Li ; KewalRamani, Vineet N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c612t-d00e71f678bd4ec1e64003ccb90fe490b71772b35dea627bfe656efc7dda731e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Antigens</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Cell Adhesion Molecules - immunology</topic><topic>Chemokines</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - immunology</topic><topic>Disease transmission</topic><topic>Drug resistance</topic><topic>Health aspects</topic><topic>HIV</topic><topic>HIV (Viruses)</topic><topic>HIV - immunology</topic><topic>HIV Infections - immunology</topic><topic>HIV Infections - transmission</topic><topic>HIV Infections - virology</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunology</topic><topic>Infections</topic><topic>Lectins, C-Type - immunology</topic><topic>Lymphocytes</topic><topic>Pathogenesis</topic><topic>Receptors, Cell Surface - immunology</topic><topic>review-article</topic><topic>Viral infections</topic><topic>Virus Internalization</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Li</creatorcontrib><creatorcontrib>KewalRamani, Vineet N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature Reviews: Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Li</au><au>KewalRamani, Vineet N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dendritic-cell interactions with HIV: infection and viral dissemination</atitle><jtitle>Nature Reviews: Immunology</jtitle><stitle>Nat Rev Immunol</stitle><addtitle>Nat Rev Immunol</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>6</volume><issue>11</issue><spage>859</spage><epage>868</epage><pages>859-868</pages><issn>1474-1733</issn><eissn>1474-1741</eissn><eissn>1365-2567</eissn><abstract>Key Points
Dendritic cells (DCs) are located in the mucosae and the lymphoid tissues. They are proposed to be among the first cells to encounter HIV during sexual transmission.
The main populations of DCs include myeloid DCs and plasmacytoid DCs in the blood, and Langerhans cells in the tissues. Myeloid DCs, plasmacytoid DCs and Langerhans cells are all susceptible to infection with HIV; they can also transfer HIV to CD4
+
T cells.
Follicular DCs can trap and maintain large quantities of HIV, thereby functioning as a persistent reservoir of virus.
Immunomodulation of DCs by HIV infection is a key aspect of viral pathogenesis, particularly through the modulation or interference of the antigen-presenting function of DCs.
DCs express high levels of C-type lectins, including DC-specific intercellular adhesion molecule 3 (ICAM3)-grabbing non-integrin (DC-SIGN; also known as CD209). C-type lectins are the main HIV attachment factors at the surface of dermal and mucosal DCs.
DCs have DC-SIGN-dependent and DC-SIGN-independent mechanisms of HIV
trans
-infection of CD4
+
T cells. The efficiency of HIV transmission can be increased by maturation of DCs.
The transfer of virus from DCs to CD4
+
T cells occurs in three discrete steps. First, DCs capture and bind HIV. Second, HIV traffics within these DCs. And third, HIV is transferred to CD4
+
T cells by a process that is known as
trans
-infection.
DC-mediated HIV
trans
-infection might occur by several distinct processes that can take place concurrently, including rapid HIV
trans
-infection through infectious synapses and exosome-associated viruses. HIV transmission can also be mediated by
de novo
viral production in DCs, known as
cis
-infection.
Elucidating the interactions of HIV with DCs will be vital to uncover the contribution of DCs to viral pathogenesis.
HIV has evolved ways to exploit dendritic cells to facilitate spread of the virus through the body. Dendritic cells can mediate the transfer of HIV to target CD4
+
T cells through several distinct mechanisms, as discussed in this Review.
Dendritic cells (DCs) are crucial for the generation and the regulation of adaptive immunity. Because DCs have a pivotal role in marshalling immune responses, HIV has evolved ways to exploit DCs, thereby facilitating viral dissemination and allowing evasion of antiviral immunity. Defining the mechanisms that underlie cell–cell transmission of HIV and understanding the role of DCs in this process should help us in the fight against HIV infection. This Review highlights the latest advances in our understanding of the interactions between DCs and HIV, focusing on the mechanisms of DC-mediated viral dissemination.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17063186</pmid><doi>10.1038/nri1960</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antigens Biomedical and Life Sciences Biomedicine CD4-Positive T-Lymphocytes - immunology Cell Adhesion Molecules - immunology Chemokines Dendritic cells Dendritic Cells - immunology Disease transmission Drug resistance Health aspects HIV HIV (Viruses) HIV - immunology HIV Infections - immunology HIV Infections - transmission HIV Infections - virology Human immunodeficiency virus Humans Immune response Immunology Infections Lectins, C-Type - immunology Lymphocytes Pathogenesis Receptors, Cell Surface - immunology review-article Viral infections Virus Internalization |
title | Dendritic-cell interactions with HIV: infection and viral dissemination |
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