To the knowledge of the 20GYGFG24 sequence stretch of type-1 VDAC: To understand why BCl-XL B4 domain peptides keep HeLa cells closed in hypotonic surroundings

2012 ◽  
Vol 106 (2) ◽  
pp. 253-254 ◽  
Author(s):  
Friedrich P. Thinnes
Keyword(s):  
Hela Cells ◽  
Sequence Stretch

scholarly journals Cellular miR-101-1 Reduces Efficiently the Replication of HSV-1 in HeLa Cells

Intervirology ◽  
2021 ◽  
Vol 64 (2) ◽  
pp. 88-95
Author(s):  
Bahar Sadegh Ehdaei ◽  
Ahmad Pirouzmand ◽  
Mehdi Shabani ◽  
Arezoo Mirzaei ◽  
Sharareh Moghim
Keyword(s):  
Hela Cells ◽  
Plaque Assay ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Herpes Simplex Viruses ◽  
Viral Progeny ◽  
Immunosuppressed Patients ◽  
Health Complications ◽  
Hsv 1

<b><i>Introduction:</i></b> Herpes simplex viruses (HSVs) are widely distributed in the human population. HSV type 1 (HSV-1) is responsible for a spectrum of diseases, ranging from gingivostomatitis to keratoconjunctivitis, and encephalitis. The HSVs establish latent infections in nerve cells, and recurrences are common. Their frequent reactivation in elderly and immunosuppressed patients causes serious health complications. <b><i>Objectives:</i></b> Due to the growing resistance to its main drug, acyclovir, alternative treatments with different mechanisms of action are required. MicroRNAs regulate host and viral gene expression posttranscriptionally. Previous studies reported that mir-101-2 expression has widely participated in the regulation of HSV-1 replication. In this study, we investigate the effect of hsa-miR-101-1 in the replication of HSV-1. <b><i>Methods:</i></b> We found that transfection of miR-101-1 into HeLa cells could reduce effectively HSV-1 replication using plaque assay and real-time PCR methods. <b><i>Results:</i></b> We showed that overexpression of miR-10-1 produced less viral progeny and manifested a weaker cytopathic effect, without affecting cell viability. <b><i>Discussion/Conclusion:</i></b> This result can give us new insights into the control of HSV-1 infections.

The type-1 ribosome-inactivating protein OsRIP1 triggers caspase-independent apoptotic-like death in HeLa cells

2021 ◽  
Vol 157 ◽  
pp. 112590
Author(s):  
Simin Chen ◽  
Cláudia Figueiredo Lóssio ◽  
Isabel Verbeke ◽  
Joost Verduijn ◽  
Bogdan Parakhonskiy ◽  
...  
Keyword(s):  
Hela Cells ◽  
Ribosome Inactivating Protein

Poliovirus type 1 capsid polypeptides: Absence of a free form in the cytoplasm of infected HeLa cells

1983 ◽  
Vol 134 (2) ◽  
pp. 151-164 ◽  
Author(s):  
P. Bruneau ◽  
B. Blondel ◽  
R. Crainic ◽  
F. Horodniceanu ◽  
M. Girard
Keyword(s):  
Hela Cells ◽  
Free Form ◽  
Poliovirus Type

scholarly journals Differential Sensitivity of “Old” versus “New” APOBEC3G to Human Immunodeficiency Virus Type 1 Vif

2008 ◽  
Vol 83 (2) ◽  
pp. 1156-1160 ◽  
Author(s):  
Ritu Goila-Gaur ◽  
Mohammad A. Khan ◽  
Eri Miyagi ◽  
Klaus Strebel
Keyword(s):  
Human Immunodeficiency Virus ◽  
Antiviral Activity ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Hela Cells ◽  
Relative Sensitivity ◽  
Differential Sensitivity ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT HIV-1 Vif counteracts the antiviral activity of APOBEC3G by inhibiting its encapsidation into virions. Here, we compared the relative sensitivity to Vif of APOBEC3G in stable HeLa cells containing APOBEC3G (HeLa-A3G cells) versus that of newly synthesized APOBEC3G. We observed that newly synthesized APOBEC3G was more sensitive to degradation than preexisting APOBEC3G. Nevertheless, preexisting and transiently expressed APOBEC3G were packaged with similar efficiencies into vif-deficient human immunodeficiency virus type 1 (HIV-1) virions, and Vif inhibited the encapsidation of both forms of APOBEC3G into HIV particles equally well. Our results suggest that HIV-1 Vif preferentially induces degradation of newly synthesized APOBEC3G but indiscriminately inhibits encapsidation of “old” and “new” APOBEC3G.

Scopadulciol is an Inhibitor of Herpes Simplex Virus Type 1 and a Potentiator of Aciclovir

1996 ◽  
Vol 7 (2) ◽  
pp. 79-85 ◽  
Author(s):  
Kyoko Hayashi ◽  
Toshimitsu Hayashi
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Antiviral Activity ◽  
Virus Type ◽  
Hela Cells ◽  
Herpes Simplex Virus Type ◽  
Infected Cells ◽  
Simplex Virus ◽  
Hsv 1

The antiviral activity of scopadulciol (SDC), a tetracyclic diterpenoid with a chemical structure related to that of aphidicolin, isolated from Scoparia dulcis, was studied in vitro against herpes simplex virus type 1 (HSV-1). SDC was found to inhibit the virus replication as shown by reduction of virus production. The action was not due to the inhibition of viral DNA polymerase activity and virus penetration, but might involve, at least in part, a virucidal effect. SDC did not suppress the viral protein synthesis of infected cells when added at an early stage of HSV-1 replication, but did when added later. When aciclovir (ACV) and SDC were evaluated in combination for antiviral activity against HSV-1 replication and cytotoxicity, these drugs inhibited viral replication in HeLa cells synergistically, but the same combination did not produce synergistic cytotoxicity in HeLa cells. Studies of the deoxynucleotide pool sizes revealed that SDC increased the intracellular dNTP pools and ACV triphosphate level significantly in infected cells when the cells were treated with the combination. These results could account for the synergistic action between SDC and ACV.

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