0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Grand Rounds |

Hepatitis C Virus Infection and Coinfection With Human Immunodeficiency Virus:  Challenges and Advancements in Management

Colleen Hadigan, MD, MPH; Shyamasundaran Kottilil, MD, PhD
JAMA. 2011;306(3):294-301. doi:10.1001/jama.2011.975.
Text Size: A A A
Published online

Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) both emerged in the second half of the 20th century, and chronic infection with these agents is among the greatest challenges facing health care in the United States and worldwide. Despite tremendous advances in treatment and management of HIV and HCV, individuals with HIV/HCV coinfection experience a more complicated disease course and treatment. Recognition of the important role that host factors, such as IL28B genotype, have in response to HCV therapy and the emergence of new effective therapies for HCV are actively reshaping the standard of care. These advances may translate into more effective treatment and management of patients with chronic HCV and HIV coinfection in the years ahead.

Figures in this Article

Sign in

Create a free personal account to sign up for alerts, share articles, and more.

Purchase Options

• Buy this article
• Subscribe to the journal

First Page Preview

View Large
First page PDF preview

Figures

Place holder to copy figure label and caption
Figure 1. Histopathology Results From Case Patient’s Percutaneous Liver Biopsy Specimens
Graphic Jump Location

A, From a biopsy in 2008, hematoxylin-eosin stain demonstrates moderate portal inflammation, moderate interface hepatitis, and mild steatosis, and Masson stain shows bridging fibrosis (blue). B, Repeat biopsy in 2010 shows hematoxylin-eosin stain demonstrating decreased inflammation and decreased steatosis, and Masson stain showing fibrosis (blue), which is unchanged. Original magnification ×200.

Place holder to copy figure label and caption
Figure 2. Target of Nonstructural 3/4A Serine Protease Inhibitors in the HCV Life Cycle
Graphic Jump Location

Nonstructural 3/4A (NS3/4A) serine protease inhibitors are directly acting antiviral agents that interfere with viral NS3 serine protease and its cofactor, NS4A. In the hepatitis C virus (HCV) life cycle, viral NS3/4A serine protease cleaves the HCV polyprotein into small nonstructural proteins that are necessary for viral replication within the hepatocyte. Two drugs in this class, telaprevir and boceprevir, were recently approved by the US Food and Drug administration. ssRNA indicates single-stranded RNA.

Tables

References

CME


You need to register in order to view this quiz.

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Web of Science® Times Cited: 22

Sign in

Create a free personal account to sign up for alerts, share articles, and more.

Purchase Options

• Buy this article
• Subscribe to the journal

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
PubMed Articles
Jobs
JAMAevidence.com
brightcove.createExperiences();