Rene Sugar

Efficacy and toxicity of hydroxyurea in mast cell activation syndrome patients refractory to standard medical therapy: retrospective case series #MCAS #MECFS #LongCovid

pmc.ncbi.nlm.nih.gov/articles/PMC...

Contrasting effects of hydroxyurea on cell growth and reduction in Epstein‐Barr virus genomes in EBV‐infected epithelioid cell lines vs. Burkitt's lymphoma cell lines Eliminating Epstein-Barr virus (EBV) genomes from infected cells is an intriguing theoretical strategy in therapy for EBV-associated malignant diseases. Respective patterns were characterized for hyd....

Contrasting effects of hydroxyurea on cell growth and reduction in Epstein-Barr virus genomes in EBV-infected epithelioid cell lines vs. Burkitt's lymphoma cell lines

onlinelibrary.wiley.com/doi/abs/10.1...

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

pubmed.ncbi.nlm.nih.gov/9593003/

"The altered growth phenotype of both BL cells and immortalized primary B cells suggests that latent EBV is an appropriate and accessible therapeutic target for treatment of some EBV-induced lymphoproliferations."

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

pubmed.ncbi.nlm.nih.gov/9593003/

"Hydroxyurea-treated primary B lymphocytes immortalized by EBV ceased to proliferate as episomes were lost."

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

pubmed.ncbi.nlm.nih.gov/9593003/

"Unlike parental EBV-positive BL cells, virus-free cell progeny from one treated cell line no longer exhibited the malignant phenotype in tumorigenicity assays."

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

pubmed.ncbi.nlm.nih.gov/9593003/

"providing the first example of chemotherapeutic eradication of a latent herpesvirus from any cell population."

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

pubmed.ncbi.nlm.nih.gov/9593003/

"In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated Epstein-Barr virus (EBV) episomes from latently infected Burkitt's lymphoma (BL) cell subsets,"

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

pubmed.ncbi.nlm.nih.gov/9593003/

"The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus."

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype - PubMed The hallmark of infection by human herpesviruses, life-long persistence in the host, is unaffected by current antiviral therapies effective against replication of virus. In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated E …

Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype #EBV #MECFS #LongCovid

pubmed.ncbi.nlm.nih.gov/9593003/

Scientists create cartilage scaffold that helps the body regrow bone Researchers in Sweden have engineered a cell-free cartilage scaffold that can guide the body to rebuild damaged bone. By removing the cells but preserving the structure and natural growth signals, the...

Scientists create cartilage scaffold that helps the body regrow bone

flip.it/ZDRTXd

Autoantibodies against type I IFNs in patients with life-threatening COVID-19 In a large immunological and genomics study of COVID-19 patients, autoantibodies to type 1 interferons correlated with outcomes.

Autoantibodies against type I IFNs in patients with life-threatening COVID-19

science.sciencemag.org/content/370/...

Inborn errors of type I IFN immunity in patients with life-threatening COVID-19 A large immunological and genomics study of COVID-19 patients reveals excess mutations in the type I IFN pathway.

Inborn errors of type I IFN immunity in patients with life-threatening COVID-19

pmc.ncbi.nlm.nih.gov/articles/PMC...

Autoantibodies against type I interferons correlate with low CD169/SIGLEC1 and severe non-viral infections in ER patients - PubMed Neutralizing autoantibodies against type I interferons are a risk factor for multiple severe viral diseases. The timely detection of these autoantibodies remains an unmet need. We hypothesized that paradoxically low expression of type I IFN-induced CD169/SIGLEC1 expression analyzed by flow cytometry …

Autoantibodies against type I interferons correlate with low CD169/SIGLEC1 and severe non-viral infections in ER patients

pubmed.ncbi.nlm.nih.gov/41329209/

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"This is a unique example of convergent evolution resulting in enhanced immune evasion of important pathogens via utilization of a “superevasion site.”"

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"Binding via this site not only mimics the glycosaminoglycans of the host cells, but also enhances function of FH on the microbial surfaces via the novel mechanism of tripartite complex formation."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"In this study we reveal that seven microbes representing different phyla utilize a common binding site on the domain 20 of FH for complement evasion."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"Surprisingly, the microbial proteins enhanced binding of FH19-20 to C3b and down-regulation of complement activation."

"We show that this is caused by formation of a tripartite complex between the microbial protein, FH, and C3b."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"Binding of FH to the microbial proteins was inhibited with heparin showing that the common microbial binding site overlaps with the heparin site needed for efficient binding of FH to host cells."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"We show that all studied microbes use the same binding region located on one side of domain 20."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"and whole microbes (Haemophilus influenzae, Bordetella pertussis, Pseudomonas aeruginosa, Streptococcus pneumonia, Candida albicans, Borrelia burgdorferi, and Borrelia hermsii)."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"We used a selection of FH19-20 point mutants to reveal the binding sites of several microbial proteins"

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"Many pathogenic microbes protect themselves from complement by recruiting host FH."

"We analyzed how and why different microbes bind FH via domains 19–20 (FH19-20)."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"FH binds simultaneously to host cell surface structures such as heparin or glycosaminoglycans via domain 20 and to the main complement opsonin C3b via domain 19."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"It can attack all kinds of targets and is tightly controlled in plasma and on host cells by plasma complement regulator factor H (FH)."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement."

Microbes Bind Complement Inhibitor Factor H via a Common Site To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in ...

Microbes Bind Complement Inhibitor Factor H via a Common Site #MECFS #LongCovid

pmc.ncbi.nlm.nih.gov/articles/PMC...

Altered increase in STAT1 expression and phosphorylation in severe COVID‐19 Anomalous upregulation of STAT1 and IRF9 (key components of IFN signaling) in B and T cells and monocytes from patients with severe COVID-19, with absence of pSTAT1 upregulation upon IFN restimulatio....

Altered increase in STAT1 expression and phosphorylation in severe COVID-19

onlinelibrary.wiley.com/doi/10.1002/...

"Both Siglec-1 and STAT1 were lower among severely affected COVID-19 patients compared to mildly affected COVID-19 patients"

Type I and II Interferon Signature Quantitation in Monocytes by Flow Cytometry
T1A2MP

www.testmenu.com/nationwidech...

CD169/SIGLEC1 is expressed on circulating monocytes in COVID-19 and expression levels are associated with disease severity Coronavirus disease 2019 (COVID-19) is caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Type I interferons are important in the defense of viral infections. Recently, neutralizing IgG auto-antibodies against ...

pmc.ncbi.nlm.nih.gov/articles/PMC...

"Activation of the type I interferon pathway rapidly increases the expression of CD169 on the surface of monocytes and macrophages."

CD169/SIGLEC1 is expressed on circulating monocytes in COVID-19 and expression levels are associated with disease severity Coronavirus disease 2019 (COVID-19) is caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Type I interferons are important in the defense of viral infections. Recently, neutralizing IgG auto-antibodies against ...

CD169/SIGLEC1 is expressed on circulating monocytes in #COVID19 and expression levels are associated with disease severity #MECFS #LongCovid

pmc.ncbi.nlm.nih.gov/articles/PMC...