Related Experiment Video

Updated: Jun 27, 2026

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
09:29

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds

Published on: October 29, 2015

Inhibition of cyclooxygenase activity blocks cell-to-cell spread of human cytomegalovirus

Jörg Schröer1, Thomas Shenk

  • 1Department of Molecular Biology, Princeton University, Princeton, NJ 08540, USA.

Proceedings of the National Academy of Sciences of the United States of America
|November 27, 2008
PubMed

Insights

Nonsteroidal anti-inflammatory drugs, like tolfenamic acid and indomethacin, can inhibit human cytomegalovirus (HCMV) cell-to-cell spread. This finding suggests NSAIDs may aid in controlling HCMV infections when used with other antiviral therapies.

Area of Science:

  • Virology
  • Pharmacology
  • Immunology

Background:

  • Human cytomegalovirus (HCMV) increases cyclooxygenase-2 (COX-2) RNA, protein, and activity.
  • High doses of COX inhibitors significantly impede viral replication in fibroblasts.
  • Therapeutic drug levels of COX inhibitors have minimal impact on HCMV replication in cell cultures.

Purpose of the Study:

  • To investigate the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on human cytomegalovirus (HCMV) spread.
  • To determine if NSAIDs can inhibit HCMV cell-to-cell transmission.
  • To explore the potential of NSAIDs in managing HCMV infections.

Main Methods:

  • Utilized cultured fibroblasts to study HCMV replication and spread.
  • Administered NSAIDs, specifically tolfenamic acid and indomethacin, to infected cell cultures.
  • Assessed viral spread inhibition and reversed effects with prostaglandin E2.

Main Results:

  • Tolfenamic acid and indomethacin significantly reduced direct cell-to-cell spread of HCMV in fibroblasts.
  • The observed inhibition of viral spread was reversed by the addition of prostaglandin E2.
  • This indicates the effect is mediated through cyclooxygenase activity.

Conclusions:

  • NSAIDs, acting via cyclooxygenase inhibition, effectively reduce HCMV cell-to-cell spread.
  • Cell-to-cell spread is a significant factor in HCMV pathogenesis.
  • NSAIDs may be a valuable adjunct therapy for controlling HCMV infections alongside other antivirals.

More Related Videos

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Related Concept Videos

Cytomegalovirus Disease01:27

Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...