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Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
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...
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
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...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...

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Related Experiment Video

Updated: Jul 13, 2026

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors
16:49

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

Pathogenesis of HIV-HCV Coinfection.

Arthur Y Kim1, Georg M Lauer

  • 1Infectious Disease Unit and Partners AIDS Research Center, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA.

Current Infectious Disease Reports
|July 10, 2007
PubMed
Summary

Hepatitis C virus (HCV) and Human Immunodeficiency Virus type 1 (HIV-1) coinfection worsens liver disease and impairs immune recovery. Understanding these interactions is key to developing new treatments for coinfected patients.

Area of Science:

  • * Virology and Immunology
  • * Hepatology and Infectious Diseases

Background:

  • * Hepatitis C virus (HCV) and Human Immunodeficiency Virus type 1 (HIV-1) frequently coexist in the same host, leading to chronic infections with persistent viremia.
  • * HIV-1 infection exacerbates HCV infection, increasing viral persistence, RNA levels, and the rate of liver fibrosis progression.
  • * HCV infection can hinder immune system recovery in HIV-1 positive individuals undergoing antiretroviral therapy.

Purpose of the Study:

  • * To elucidate the pathogenic mechanisms driving the clinical manifestations of HIV/HCV coinfection.
  • * To identify potential targets for novel therapeutic interventions against HIV/HCV coinfection.

Main Methods:

  • * Review and analysis of existing literature on HIV-HCV interactions.
  • * Examination of immunological and virological data from coinfected patients.

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Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
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Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis

Published on: September 11, 2019

Related Experiment Videos

Last Updated: Jul 13, 2026

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors
16:49

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

A Protocol for Analyzing Hepatitis C Virus Replication
13:04

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
10:12

Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis

Published on: September 11, 2019

Main Results:

  • * HIV-1 accelerates HCV-related liver fibrosis and increases viral load.
  • * HCV negatively impacts immune reconstitution in HIV-1 patients on antiretroviral therapy.
  • * Complex interplay between viral dynamics and host immune responses observed.

Conclusions:

  • * Understanding the mechanisms of HIV-HCV coinfection is crucial for clinical management.
  • * Targeting these pathogenic pathways may lead to improved therapeutic strategies for coinfected individuals.