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Article ; Online: Specific plasma microRNAs are associated with CD4 + T-cell recovery during suppressive antiretroviral therapy for HIV-1.

Kroeze, Stefanie / Kootstra, Neeltje A / van Nuenen, Ad C / Rossouw, Theresa M / Kityo, Cissy M / Siwale, Margaret / Akanmu, Sulaimon / Mandaliya, Kishor / de Jager, Marleen / Ondoa, Pascale / Wit, Ferdinand W / Reiss, Peter / Rinke de Wit, Tobias F / Hamers, Raph L

AIDS (London, England)

2024 Volume 38, Issue 6, Page(s) 791–801

Abstract: Objective: This study investigated the association of plasma microRNAs before and during antiretroviral therapy (ART) with poor CD4 + T-cell recovery during the first year of ART.: Design: MicroRNAs were retrospectively measured in stored plasma ... ...

Abstract	Objective: This study investigated the association of plasma microRNAs before and during antiretroviral therapy (ART) with poor CD4 + T-cell recovery during the first year of ART. Design: MicroRNAs were retrospectively measured in stored plasma samples from people with HIV (PWH) in sub-Saharan Africa who were enrolled in a longitudinal multicountry cohort and who had plasma viral-load less than 50 copies/ml after 12 months of ART. Methods: First, the levels of 179 microRNAs were screened in a subset of participants from the lowest and highest tertiles of CD4 + T-cell recovery (ΔCD4) ( N = 12 each). Next, 11 discordant microRNAs, were validated in 113 participants (lowest tertile ΔCD4: n = 61, highest tertile ΔCD4: n = 52). For discordant microRNAs in the validation, a pathway analysis was conducted. Lastly, we compared microRNA levels of PWH to HIV-negative controls. Results: Poor CD4 + T-cell recovery was associated with higher levels of hsa-miR-199a-3p and hsa-miR-200c-3p before ART, and of hsa-miR-17-5p and hsa-miR-501-3p during ART. Signaling by VEGF and MET, and RNA polymerase II transcription pathways were identified as possible targets of hsa-miR-199a-3p, hsa-200c-3p, and hsa-miR-17-5p. Compared with HIV-negative controls, we observed lower hsa-miR-326, hsa-miR-497-5p, and hsa-miR-501-3p levels before and during ART in all PWH, and higher hsa-miR-199a-3p and hsa-miR-200c-3p levels before ART in all PWH, and during ART in PWH with poor CD4 + T-cell recovery only. Conclusion: These findings add to the understanding of pathways involved in persistent HIV-induced immune dysregulation during suppressive ART.
MeSH term(s)	Humans ; HIV-1/genetics ; Retrospective Studies ; HIV Infections/drug therapy ; MicroRNAs/genetics ; T-Lymphocytes
Chemical Substances	MicroRNAs ; MIRN326 microRNA, human ; MIRN497 microRNA, human
Language	English
Publishing date	2024-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0000000000003853
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Article ; Online: SARS-CoV-2 suppresses TLR4-induced immunity by dendritic cells via C-type lectin receptor DC-SIGN.

van der Donk, Lieve E H / Bermejo-Jambrina, Marta / van Hamme, John L / Volkers, Mette M W / van Nuenen, Ad C / Kootstra, Neeltje A / Geijtenbeek, Teunis B H

PLoS pathogens

2023 Volume 19, Issue 10, Page(s) e1011735

Abstract: SARS-CoV-2 causes COVID-19, an infectious disease with symptoms ranging from a mild cold to severe pneumonia, inflammation, and even death. Although strong inflammatory responses are a major factor in causing morbidity and mortality, superinfections with ...

Abstract	SARS-CoV-2 causes COVID-19, an infectious disease with symptoms ranging from a mild cold to severe pneumonia, inflammation, and even death. Although strong inflammatory responses are a major factor in causing morbidity and mortality, superinfections with bacteria during severe COVID-19 often cause pneumonia, bacteremia and sepsis. Aberrant immune responses might underlie increased sensitivity to bacteria during COVID-19 but the mechanisms remain unclear. Here we investigated whether SARS-CoV-2 directly suppresses immune responses to bacteria. We studied the functionality of human dendritic cells (DCs) towards a variety of bacterial triggers after exposure to SARS-CoV-2 Spike (S) protein and SARS-CoV-2 primary isolate (hCoV-19/Italy). Notably, pre-exposure of DCs to either SARS-CoV-2 S protein or a SARS-CoV-2 isolate led to reduced type I interferon (IFN) and cytokine responses in response to Toll-like receptor (TLR)4 agonist lipopolysaccharide (LPS), whereas other TLR agonists were not affected. SARS-CoV-2 S protein interacted with the C-type lectin receptor DC-SIGN and, notably, blocking DC-SIGN with antibodies restored type I IFN and cytokine responses to LPS. Moreover, blocking the kinase Raf-1 by a small molecule inhibitor restored immune responses to LPS. These results suggest that SARS-CoV-2 modulates DC function upon TLR4 triggering via DC-SIGN-induced Raf-1 pathway. These data imply that SARS-CoV-2 actively suppresses DC function via DC-SIGN, which might account for the higher mortality rates observed in patients with COVID-19 and bacterial superinfections.
MeSH term(s)	Humans ; SARS-CoV-2/metabolism ; Toll-Like Receptor 4/metabolism ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/metabolism ; Superinfection ; COVID-19/metabolism ; Lectins, C-Type/metabolism ; Cytokines/metabolism ; Dendritic Cells
Chemical Substances	DC-specific ICAM-3 grabbing nonintegrin ; spike protein, SARS-CoV-2 ; Toll-Like Receptor 4 ; Lipopolysaccharides ; Lectins, C-Type ; Cytokines ; TLR4 protein, human
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1011735
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Article ; Online: Nef Obtained from Individuals with HIV-1 Vary in Their Ability to Antagonize SERINC3- and SERINC5-Mediated HIV-1 Restriction.

Kruize, Zita / van Nuenen, Ad C / van Wijk, Stan W / Girigorie, Arginell F / van Dort, Karel A / Booiman, Thijs / Kootstra, Neeltje A

Viruses

2021 Volume 13, Issue 3

Abstract: Nef is a multifunctional viral protein that has the ability to downregulate cell surface molecules, including CD4 and major histocompatibility complex class I (MHC-I) and, as recently shown, also members of the serine incorporator family (SERINC). Here, ... ...

Abstract	Nef is a multifunctional viral protein that has the ability to downregulate cell surface molecules, including CD4 and major histocompatibility complex class I (MHC-I) and, as recently shown, also members of the serine incorporator family (SERINC). Here, we analyzed the impact of naturally occurring mutations in HIV-1 Nef on its ability to counteract SERINC restriction and the clinical course of infection. HIV-1 Nef sequences were obtained from 123 participants of the Amsterdam Cohort Studies and showed multiple amino acid variations and mutations. Most of the primary Nef proteins showed increased activity to counteract SERINC3 and SERINC5 as compared to NL4-3 Nef. Several mutations in Nef were associated with either an increased or decreased infectivity of Bal26-pseudotyped HIV-1 produced in the presence of SERINC3 or SERINC5. The 8R, 157N and R178G Nef mutations were shown to have an effect on disease progression. Survival analysis showed an accelerated disease progression of individuals infected with HIV-1 carrying arginine or asparagine at position 8 or 157 in Nef, respectively, or the R178G Nef mutation. Here, we observed that naturally occurring mutations in Nef affect the ability of Nef to counteract SERINC3- and SERINC5-mediated inhibition of viral infectivity. The majority of these Nef mutations had no significant effect on HIV-1 pathogenesis and only the 8R, 157N and R178G mutations were associated with disease course.
MeSH term(s)	Cohort Studies ; HIV Infections/virology ; HIV-1/genetics ; HIV-1/immunology ; Host Microbial Interactions ; Humans ; Male ; Membrane Glycoproteins/immunology ; Membrane Proteins/immunology ; Mutation ; Netherlands ; Sexual and Gender Minorities ; nef Gene Products, Human Immunodeficiency Virus/genetics
Chemical Substances	Membrane Glycoproteins ; Membrane Proteins ; SERINC3 protein, human ; SERINC5 protein, human ; nef Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2021-03-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v13030423
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Article: Nef Obtained from Individuals with HIV-1 Vary in Their Ability to Antagonize SERINC3- and SERINC5-Mediated HIV-1 Restriction

Kruize, Zita / van Nuenen, Ad C / van Wijk, Stan W / Girigorie, Arginell F / van Dort, Karel A / Booiman, Thijs / Kootstra, Neeltje A

Viruses. 2021 Mar. 06, v. 13, no. 3

2021

Abstract	Nef is a multifunctional viral protein that has the ability to downregulate cell surface molecules, including CD4 and major histocompatibility complex class I (MHC-I) and, as recently shown, also members of the serine incorporator family (SERINC). Here, we analyzed the impact of naturally occurring mutations in HIV-1 Nef on its ability to counteract SERINC restriction and the clinical course of infection. HIV-1 Nef sequences were obtained from 123 participants of the Amsterdam Cohort Studies and showed multiple amino acid variations and mutations. Most of the primary Nef proteins showed increased activity to counteract SERINC3 and SERINC5 as compared to NL4-3 Nef. Several mutations in Nef were associated with either an increased or decreased infectivity of Bal26-pseudotyped HIV-1 produced in the presence of SERINC3 or SERINC5. The 8R, 157N and R178G Nef mutations were shown to have an effect on disease progression. Survival analysis showed an accelerated disease progression of individuals infected with HIV-1 carrying arginine or asparagine at position 8 or 157 in Nef, respectively, or the R178G Nef mutation. Here, we observed that naturally occurring mutations in Nef affect the ability of Nef to counteract SERINC3- and SERINC5-mediated inhibition of viral infectivity. The majority of these Nef mutations had no significant effect on HIV-1 pathogenesis and only the 8R, 157N and R178G mutations were associated with disease course.
Keywords	arginine ; asparagine ; disease course ; disease progression ; major histocompatibility complex ; mutation ; pathogenesis ; pathogenicity ; serine
Language	English
Dates of publication	2021-0306
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-light
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v13030423
Database	NAL-Catalogue (AGRICOLA)

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Article: CD9 and ITGA3 are regulated during HIV-1 infection in macrophages to support viral replication

Kruize, Zita / Cobos Jiménez, Viviana / Martinez, Fernando O. / Di Vincenzo, Riccardo / van Dort, Karel A. / van Nuenen, Ad C. / Booiman, Thijs / Kootstra, Neeltje A.

Virology. 2021 Oct., v. 562

2021

Abstract: Monocytes/macrophages are important target cells for HIV-1. Here, we investigated whether HIV-1 induces changes in the macrophage gene expression profile to support viral replication.We observed that the macrophage gene expression profiles dramatically ... ...

Abstract	Monocytes/macrophages are important target cells for HIV-1. Here, we investigated whether HIV-1 induces changes in the macrophage gene expression profile to support viral replication.We observed that the macrophage gene expression profiles dramatically changed upon HIV-1 infection. The majority of the HIV-1 regulated genes were also differentially expressed in M2a macrophages. The biological functions associated with the HIV-1 induced gene expression profile in macrophages were mainly related to inflammatory responses. CD9 and ITGA3 were among the top genes upregulated upon HIV-1 infection. We showed that these genes support viral replication and that downregulation of these genes decreased HIV-1 replication in macrophages.Here we showed that HIV-1 infection of macrophages induces a gene expression profile that may dampen inflammatory responses. CD9 and ITGA3 were among the top genes regulated by HIV-1 and were shown to support viral production most likely at the level of viral budding and release.
Keywords	HIV infections ; gene expression ; macrophages ; monocytes ; virus replication
Language	English
Dates of publication	2021-10
Size	p. 9-18.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2021.07.002
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Article ; Online: Identification of 2-(4-N,N-Dimethylaminophenyl)-5-methyl-1-phenethyl-1H-benzimidazole targeting HIV-1 CA capsid protein and inhibiting HIV-1 replication in cellulo.

Alvarez, Guzmán / van Pul, Lisa / Robert, Xavier / Artía, Zoraima / van Nuenen, Ad C / Long, Mathieu / Sierra, Natalia / Porcal, Williams / Kootstra, Neeltje A / Guillon, Christophe

BMC pharmacology & toxicology

2022 Volume 23, Issue 1, Page(s) 43

Abstract: The capsid (CA) subunit of the HIV-1 Gag polyprotein is involved in several steps of the viral cycle, from the assembly of new viral particles to the protection of the viral genome until it enters into the nucleus of newly infected cells. As such, it ... ...

Abstract	The capsid (CA) subunit of the HIV-1 Gag polyprotein is involved in several steps of the viral cycle, from the assembly of new viral particles to the protection of the viral genome until it enters into the nucleus of newly infected cells. As such, it represents an interesting therapeutic target to tackle HIV infection. In this study, we screened hundreds of compounds with a low cost of synthesis for their ability to interfere with Gag assembly in vitro. Representatives of the most promising families of compounds were then tested for their ability to inhibit HIV-1 replication in cellulo. From these molecules, a hit compound from the benzimidazole family with high metabolic stability and low toxicity, 2-(4-N,N-dimethylaminophenyl)-5-methyl-1-phenethyl-1H-benzimidazole (696), appeared to block HIV-1 replication with an IC50 of 3 µM. Quantitative PCR experiments demonstrated that 696 does not block HIV-1 infection before the end of reverse transcription, and molecular docking confirmed that 696 is likely to bind at the interface between two monomers of CA and interfere with capsid oligomerization. Altogether, 696 represents a promising lead molecule for the development of a new series of HIV-1 inhibitors.
MeSH term(s)	Benzimidazoles/pharmacology ; Capsid Proteins ; HIV Infections ; HIV-1 ; Humans ; Molecular Docking Simulation ; Virus Replication
Chemical Substances	Benzimidazoles ; Capsid Proteins
Language	English
Publishing date	2022-06-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2680259-4
ISSN	2050-6511 ; 2050-6511
ISSN (online)	2050-6511
ISSN	2050-6511
DOI	10.1186/s40360-022-00581-7
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Article ; Online: SARS-CoV-2 infection activates dendritic cells via cytosolic receptors rather than extracellular TLRs.

van der Donk, Lieve E H / Eder, Julia / van Hamme, John L / Brouwer, Philip J M / Brinkkemper, Mitch / van Nuenen, Ad C / van Gils, Marit J / Sanders, Rogier W / Kootstra, Neeltje A / Bermejo-Jambrina, Marta / Geijtenbeek, Teunis B H

European journal of immunology

2022 Volume 52, Issue 4, Page(s) 646–655

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), an infectious disease characterized by strong induction of inflammatory cytokines, progressive lung inflammation, and potentially multiorgan ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), an infectious disease characterized by strong induction of inflammatory cytokines, progressive lung inflammation, and potentially multiorgan dysfunction. It remains unclear how SARS-CoV-2 infection leads to immune activation. The Spike (S) protein of SARS-CoV-2 has been suggested to trigger TLR4 and thereby activate immunity. Here, we have investigated the role of TLR4 in SARS-CoV-2 infection and immunity. Neither exposure of isolated S protein, SARS-CoV-2 pseudovirus nor primary SARS-CoV-2 isolate induced TLR4 activation in a TLR4-expressing cell line. Human monocyte-derived DCs express TLR4 but not angiotensin converting enzyme 2 (ACE2), and DCs were not infected by SARS-CoV-2. Notably, neither S protein nor SARS-CoV-2 induced DC maturation or cytokines, indicating that both S protein and SARS-CoV-2 virus particles do not trigger extracellular TLRs including TLR4. Ectopic expression of ACE2 in DCs led to efficient infection by SARS-CoV-2 and, strikingly, efficient type I IFN and cytokine responses. These data strongly suggest that not extracellular TLRs but intracellular viral sensors are key players in sensing SARS-CoV-2. These data imply that SARS-CoV-2 escapes direct sensing by TLRs, which might underlie the lack of efficient immunity to SARS-CoV-2 early during infection.
MeSH term(s)	COVID-19/immunology ; Cell Line ; Dendritic Cells/immunology ; Humans ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/immunology ; Toll-Like Receptor 4/immunology
Chemical Substances	Spike Glycoprotein, Coronavirus ; TLR4 protein, human ; Toll-Like Receptor 4 ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-02-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202149656
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: CD9 and ITGA3 are regulated during HIV-1 infection in macrophages to support viral replication.

Kruize, Zita / Cobos Jiménez, Viviana / Martinez, Fernando O / Di Vincenzo, Riccardo / van Dort, Karel A / van Nuenen, Ad C / Booiman, Thijs / Kootstra, Neeltje A

Virology

2021 Volume 562, Page(s) 9–18

Abstract: Monocytes/macrophages are important target cells for HIV-1. Here, we investigated whether HIV-1 induces changes in the macrophage gene expression profile to support viral replication. We observed that the macrophage gene expression profiles dramatically ... ...

Abstract	Monocytes/macrophages are important target cells for HIV-1. Here, we investigated whether HIV-1 induces changes in the macrophage gene expression profile to support viral replication. We observed that the macrophage gene expression profiles dramatically changed upon HIV-1 infection. The majority of the HIV-1 regulated genes were also differentially expressed in M2a macrophages. The biological functions associated with the HIV-1 induced gene expression profile in macrophages were mainly related to inflammatory responses. CD9 and ITGA3 were among the top genes upregulated upon HIV-1 infection. We showed that these genes support viral replication and that downregulation of these genes decreased HIV-1 replication in macrophages. Here we showed that HIV-1 infection of macrophages induces a gene expression profile that may dampen inflammatory responses. CD9 and ITGA3 were among the top genes regulated by HIV-1 and were shown to support viral production most likely at the level of viral budding and release.
MeSH term(s)	Gene Expression Profiling ; HIV-1/physiology ; Humans ; Integrin alpha3/genetics ; Integrin alpha3/metabolism ; Macrophages/metabolism ; Macrophages/virology ; Tetraspanin 29/genetics ; Tetraspanin 29/metabolism ; Virus Release/physiology ; Virus Replication/physiology
Chemical Substances	CD9 protein, human ; ITGA3 protein, human ; Integrin alpha3 ; Tetraspanin 29
Language	English
Publishing date	2021-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2021.07.002
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Article ; Online: Robust Vaccine-Induced as Well as Hybrid B- and T-Cell Immunity across SARS-CoV-2 Vaccine Platforms in People with HIV.

Verburgh, Myrthe L / van Pul, Lisa / Grobben, Marloes / Boyd, Anders / Wit, Ferdinand W N M / van Nuenen, Ad C / van Dort, Karel A / Tejjani, Khadija / van Rijswijk, Jacqueline / Bakker, Margreet / van der Hoek, Lia / Schim van der Loeff, Maarten F / van der Valk, Marc / van Gils, Marit J / Kootstra, Neeltje A / Reiss, Peter

Microbiology spectrum

2023 Volume 11, Issue 3, Page(s) e0115523

Abstract: Few studies have comprehensively compared severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine-induced and hybrid B- and T-cell responses in people with HIV (PWH) to those in comparable controls without HIV. We included 195 PWH and 246 ... ...

Abstract	Few studies have comprehensively compared severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine-induced and hybrid B- and T-cell responses in people with HIV (PWH) to those in comparable controls without HIV. We included 195 PWH and 246 comparable controls from the AGE
MeSH term(s)	Middle Aged ; Female ; Humans ; COVID-19 Vaccines ; CD8-Positive T-Lymphocytes ; COVID-19/prevention & control ; SARS-CoV-2 ; Vaccines ; Vaccination ; Antibodies, Viral ; Immunoglobulin A ; Immunoglobulin G ; HIV Infections
Chemical Substances	COVID-19 Vaccines ; Vaccines ; Antibodies, Viral ; Immunoglobulin A ; Immunoglobulin G
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.01155-23
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Article ; Online: Virological and immunological correlates of HIV posttreatment control after temporal antiretroviral therapy during acute HIV infection.

AIDS (London, England)

2023 Volume 37, Issue 15, Page(s) 2297–2304

Abstract: Objective: People with HIV rarely control viral replication after cessation of antiretroviral therapy (ART). We present a person with HIV with extraordinary posttreatment control (PTC) for over 23 years after temporary ART during acute HIV infection ( ... ...

Abstract	Objective: People with HIV rarely control viral replication after cessation of antiretroviral therapy (ART). We present a person with HIV with extraordinary posttreatment control (PTC) for over 23 years after temporary ART during acute HIV infection (AHI) leading to a new insight in factors contributing to PTC. Design/methods: Viral reservoir was determined by HIV qPCR, Intact Proviral DNA Assay, and quantitative viral outgrowth assay. Viral replication kinetics were determined in autologous and donor PBMC. IgG levels directed against HIV envelope and neutralizing antibodies were measured. Immune phenotyping of T cells and HIV-specific T-cell responses were analyzed by flow cytometry. Results: The case presented with AHI and a plasma viral load of 2.7 million copies/ml. ART was initiated 2 weeks after diagnosis and interrupted after 26 months. Replicating virus was isolated shortly after start ART. At 18 years after treatment interruption, HIV-DNA in CD4 + T cells and low levels of HIV-RNA in plasma (<5 copies/ml) were detectable. Stable HIV envelope glycoprotein-directed IgG was present during follow-up, but lacked neutralizing activity. Strong antiviral CD8 + T-cell responses, in particular targeting HIV-gag, were detected during 25 years follow-up. Moreover, we found a P255A mutation in an HLA-B∗44 : 02 restricted gag-epitope, which was associated with decreased replication. Conclusion: We describe an exceptional case of PTC, which is likely associated with sustained potent gag-specific CD8 + T-cell responses in combination with a replication attenuating escape mutation in gag. Understanding the initiation and preservation of the HIV-specific T-cell responses could guide the development of strategies to induce HIV control.
MeSH term(s)	Humans ; HIV Infections ; Leukocytes, Mononuclear ; CD4-Positive T-Lymphocytes ; CD8-Positive T-Lymphocytes ; DNA ; Immunoglobulin G ; Viral Load
Chemical Substances	DNA (9007-49-2) ; Immunoglobulin G
Language	English
Publishing date	2023-09-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0000000000003722
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