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1.
AIDS Res Hum Retroviruses ; 36(7): 545-549, 2020 07.
Article in English | MEDLINE | ID: covidwho-1556715

ABSTRACT

One cannot spend >5 min on social media at the moment without finding a link to some conspiracy theory or other regarding the origin of SARS-CoV2, the coronavirus responsible for the COVID-19 pandemic. From the virus being deliberately released as a bioweapon to pharmaceutical companies blocking the trials of natural remedies to boost their dangerous drugs and vaccines, the Internet is rife with far-fetched rumors. And predictably, now that the first immunization trials have started, the antivaccine lobby has latched on to most of them. In the last week, the trailer for a new "bombshell documentary" Plandemic has been doing the rounds, gaining notoriety for being repeatedly removed from YouTube and Facebook. We usually would not pay much heed to such things, but for retrovirologists like us, the name associated with these claims is unfortunately too familiar: Dr. Judy Mikovits.


Subject(s)
Betacoronavirus , Coronavirus Infections/epidemiology , Fatigue Syndrome, Chronic/virology , Fraud , Medical Laboratory Personnel/psychology , Pneumonia, Viral/epidemiology , Prostatic Neoplasms/virology , Research Personnel/psychology , Retroviridae Infections/complications , Retroviridae/physiology , Animals , COVID-19 , Coronavirus Infections/virology , Deception , Humans , Male , Mice , Pandemics , Pneumonia, Viral/virology , Retroviridae Infections/virology , SARS-CoV-2 , Social Media
2.
Nat Commun ; 12(1): 5376, 2021 09 10.
Article in English | MEDLINE | ID: covidwho-1402068

ABSTRACT

Natural killer (NK) cells are important early responders against viral infections. Changes in metabolism are crucial to fuel NK cell responses, and altered metabolism is linked to NK cell dysfunction in obesity and cancer. However, very little is known about the metabolic requirements of NK cells during acute retroviral infection and their importance for antiviral immunity. Here, using the Friend retrovirus mouse model, we show that following infection NK cells increase nutrient uptake, including amino acids and iron, and reprogram their metabolic machinery by increasing glycolysis and mitochondrial metabolism. Specific deletion of the amino acid transporter Slc7a5 has only discrete effects on NK cells, but iron deficiency profoundly impaires NK cell antiviral functions, leading to increased viral loads. Our study thus shows the requirement of nutrients and metabolism for the antiviral activity of NK cells, and has important implications for viral infections associated with altered iron levels such as HIV and SARS-CoV-2.


Subject(s)
Killer Cells, Natural/immunology , Killer Cells, Natural/metabolism , Retroviridae Infections/immunology , Animals , Bone Marrow , COVID-19 , Cytokines , HIV , HIV Infections , Large Neutral Amino Acid-Transporter 1/genetics , Large Neutral Amino Acid-Transporter 1/metabolism , Mice , Mice, Inbred C57BL , Mice, Knockout , Mitochondria , Retroviridae , Retroviridae Infections/virology , SARS-CoV-2 , Viral Load
3.
OMICS ; 25(6): 358-371, 2021 06.
Article in English | MEDLINE | ID: covidwho-1243453

ABSTRACT

About a tenth of all cancers are caused by viruses or associated with viral infection. Recent global events including the coronavirus disease-2019 (COVID-19) pandemic means that human encounter with viruses is increased. Cancer development in individuals with viral infection can take many years after infection, demonstrating that the involvement of viruses in cancer development is a long and complex process. This complexity emanates from individual genetic heterogeneity and the many steps involved in cancer development owing to viruses. The process of tumorigenesis is driven by the complex interaction between several viral factors and host factors leading to the creation of a tumor microenvironment (TME) that is ideal and promotes tumor formation. Viruses associated with human cancers ensure their survival and proliferation through activation of several cellular processes including inflammation, migration, and invasion, resistance to apoptosis and growth suppressors. In addition, most human oncoviruses evade immune detection and can activate signaling cascades including the PI3K-Akt-mTOR, Notch and Wnt pathways associated with enhanced proliferation and angiogenesis. This expert review examines and synthesizes the multiple biological factors related to oncoviruses, and the signaling cascades activated by these viruses contributing to viral oncogenesis. In particular, I examine and review the Epstein-Barr virus, human papillomaviruses, and Kaposi's sarcoma herpes virus in a context of cancer pathogenesis. I conclude with a future outlook on therapeutic targeting of the viruses and their associated oncogenic pathways within the TME. These anticancer strategies can be in the form of, but not limited to, antibodies and inhibitors.


Subject(s)
Epstein-Barr Virus Infections/virology , Neoplasms/virology , Papillomavirus Infections/virology , Retroviridae Infections/virology , Retroviridae/physiology , Sarcoma, Kaposi/virology , Tumor Virus Infections/virology , Alphapapillomavirus/physiology , Carcinogenesis , Cell Transformation, Viral , Epstein-Barr Virus Infections/pathology , Herpesvirus 4, Human/physiology , Herpesvirus 8, Human/physiology , Humans , Molecular Targeted Therapy , Neoplasms/pathology , Neoplasms/therapy , Papillomavirus Infections/pathology , Retroviridae Infections/pathology , Sarcoma, Kaposi/pathology , Signal Transduction , Tumor Microenvironment , Tumor Virus Infections/pathology
4.
Viruses ; 13(1)2021 Jan 17.
Article in English | MEDLINE | ID: covidwho-1040990

ABSTRACT

The APOBEC3 family of proteins in mammals consists of cellular cytosine deaminases and well-known restriction factors against retroviruses, including lentiviruses. APOBEC3 genes are highly amplified and diversified in mammals, suggesting that their evolution and diversification have been driven by conflicts with ancient viruses. At present, lentiviruses, including HIV, the causative agent of AIDS, are known to encode a viral protein called Vif to overcome the antiviral effects of the APOBEC3 proteins of their hosts. Recent studies have revealed that the acquisition of an anti-APOBEC3 ability by lentiviruses is a key step in achieving successful cross-species transmission. Here, we summarize the current knowledge of the interplay between mammalian APOBEC3 proteins and viral infections and introduce a scenario of the coevolution of mammalian APOBEC3 genes and viruses.


Subject(s)
APOBEC Deaminases/metabolism , Host-Pathogen Interactions , Retroviridae Infections/metabolism , Retroviridae Infections/virology , Retroviridae/physiology , APOBEC Deaminases/genetics , Animals , Disease Resistance/genetics , Evolution, Molecular , Genetic Variation , Genome, Viral , Host-Pathogen Interactions/genetics , Humans , Lentivirus/physiology , Phylogeny , Retroviridae Infections/transmission , Species Specificity , vif Gene Products, Human Immunodeficiency Virus
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