Increased CD36 Expression in Vertically Human Immunodeficiency Virus-Infected Children Unrelated to Antiretroviral Therapy

Meroni, Luca; Giacomet, Vania; Morelli, Paola; Erba, Paola; Galazzi, Morena; Riva, Agostino; Viganò, Alessandra; Galli, Massimo

doi:10.1097/01.inf.0000164800.14220.4a

Cited by 5 publications

(4 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies of CD36-null mice have shown that CD36 promotes the development of atheromas [9,10]. An increased expression of CD36 on circulating monocytes has been reported in both HIV-infected adults and children [41,42]. Our study, the first to look at the association between CD36 and IMT, shows that although CD36 is overexpressed in HIV-infected children, it is not associated with CCIMT.…”

Section: Discussionsupporting

confidence: 45%

Both HIV-Infection and Long-Term Antiretroviral Therapy are Associated with Increased Common Carotid Intima-Media Thickness in HIV-Infected Adolescents and Young Adults

Viganò¹,

Bedogni²,

Cerini³

et al. 2010

CHR

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 45%

Both HIV-Infection and Long-Term Antiretroviral Therapy are Associated with Increased Common Carotid Intima-Media Thickness in HIV-Infected Adolescents and Young Adults

Viganò¹,

Bedogni²,

Cerini³

et al. 2010

CHR

Self Cite

View full text Add to dashboard Cite

show abstract

“…CD36 plays an important role in the transport and uptake of longchain fatty acids into cells and participates in pathological processes, such as metabolic disorders and infections [44]. Previous reports showed that CD36 levels are increased in HCV and HIV-1 infections [45,46] and that it facilitates the viral attachment on host cell membrane contributing to viral replication [43]. Our results demonstrated that SARS-CoV-2 infection increases the CD36 expression in monocytes, suggesting that the increase of lipids uptake can contribute to LD formation, observed after the infection.…”

Section: Discussionmentioning

confidence: 99%

Lipid droplets fuel SARS-CoV-2 replication and production of inflammatory mediators

et al. 2020

View full text Add to dashboard Cite

Viruses are obligate intracellular parasites that make use of the host metabolic machineries to meet their biosynthetic needs. Thus, identifying the host pathways essential for the virus replication may lead to potential targets for therapeutic intervention. The mechanisms and pathways explored by SARS-CoV-2 to support its replication within host cells are not fully known. Lipid droplets (LD) are organelles with major functions in lipid metabolism, energy homeostasis and intracellular transport, and have multiple roles in infections and inflammation. Here we described that monocytes from COVID-19 patients have an increased LD accumulation compared to SARS-CoV-2 negative donors. In vitro, SARS-CoV-2 infection were seen to modulate pathways of lipid synthesis and uptake as monitored by testing for CD36, SREBP-1, PPARγ, and DGAT-1 expression in monocytes and triggered LD formation in different human cell lines. LDs were found in close apposition with SARS-CoV-2 proteins and double-stranded (ds)-RNA in infected Vero cells. Electron microscopy (EM) analysis of SARS-CoV-2 infected Vero cells show viral particles colocalizing with LDs, suggestive that LDs might serve as an assembly platform. Pharmacological modulation of LD formation by inhibition of DGAT-1 with A922500 significantly inhibited SARS-CoV-2 replication as well as reduced production of mediators pro-inflammatory response. Taken together, we demonstrate the essential role of lipid metabolic reprograming and LD formation in SARS-CoV-2 replication and pathogenesis, opening new opportunities for therapeutic strategies to COVID-19.

show abstract

“…CD36 plays an important role in the transport and uptake of long-chain fatty acids into cells and participates in pathological process, such as metabolic disorders and infections (Febbraio et al, 2001). Previous reports showed that CD36 levels are increased in HCV and HIV-1 (Berre et al, 2013;Meroni et al, 2005) infection and it facilitates the viral attachment on host cell membrane contributing to viral replication (Cheng et al, 2016). Our results demonstrated that SARS-CoV-2 infection increase the CD36 expression in monocytes, suggesting the increase of lipids uptake can contribute to LD formation, observed after the infection.…”

Section: Discussionmentioning

confidence: 99%

Lipid droplets fuel SARS-CoV-2 replication and production of inflammatory mediators

Dias

Soares

Ferreira

et al. 2020

Preprint

View full text Add to dashboard Cite

Viruses are obligate intracellular parasites that make use of the host metabolic machineries to meet their biosynthetic needs, identifying the host pathways essential for the virus replication may lead to potential targets for therapeutic intervention. The mechanisms and pathways explored by SARS-CoV-2 to support its replication within host cells are not fully known. Lipid droplets (LD) are organelles with major functions in lipid metabolism and energy homeostasis, and have multiple roles in infections and inflammation. Here we demonstrate that monocytes from COVID-19 patients have an increased LD accumulation compared to SARS-CoV-2 negative donors. In vitro, SARS-CoV-2 infection modulates pathways of lipid synthesis and uptake, as CD36, SREBP-1, PPARγ and DGAT-1 in human monocytes and triggered LD formation in different human cells. LDs were found in close apposition with SARS-CoV-2 proteins and double-stranded (ds)-RNA. The pharmacological modulation of LD formation by inhibition of DGAT-1 with A922500 significantly inhibited SARS-CoV-2 replication as well as reduced production of pro-inflammatory mediators. Taken together, we demonstrate the essential role of lipid metabolic reprograming and LD formation in SARS-CoV-2 replication and pathogenesis, opening new opportunities for therapeutic strategies to COVID-19.

show abstract

Increased CD36 Expression in Vertically Human Immunodeficiency Virus-Infected Children Unrelated to Antiretroviral Therapy

Cited by 5 publications

References 6 publications

Both HIV-Infection and Long-Term Antiretroviral Therapy are Associated with Increased Common Carotid Intima-Media Thickness in HIV-Infected Adolescents and Young Adults

Both HIV-Infection and Long-Term Antiretroviral Therapy are Associated with Increased Common Carotid Intima-Media Thickness in HIV-Infected Adolescents and Young Adults

Lipid droplets fuel SARS-CoV-2 replication and production of inflammatory mediators

Lipid droplets fuel SARS-CoV-2 replication and production of inflammatory mediators

Contact Info

Product

Resources

About