March #45 : HIV’s Incredible Endgame - by Lark Lands

POZ - Health, Life and HIV
Subscribe to:
POZ magazine
Join POZ: Facebook MySpace Twitter Pinterest
Tumblr Google+ Flickr MySpace
POZ Personals
Sign In / Join

Back to home » Archives » POZ Magazine issues

Table of Contents

Dog Days in Malibu


Born in Flames

Gay Guru

Soldier of Fortune

Rare Gem

Marathon Man

On the Waterfront

Race With the Angels

Mean Streets


To the Editor

Ticket to Ride

Death by Disclosure

Slip Off the Old Block

Poster of the Month: Ruff Times


Say What

HIV in the Hood

No Brownie Points

Grades for AIDS

French Twist

Southern Discomfort

Sister Act Up

Sister Act Up


POZarazzi: Call It a Day

Verse: Terminal Girl

Primary Concerns


Naming Names

Fast Company

Junk Mail

Life After Legacy

Spin Doctors

PWAs’ Best Friend

What’s Up, Doc?

HIV’s Incredible Endgame

The ABCs of Baby AZT

Hit the Dirt

Selling Sustiva

Publish or Perish

Best of the Rest

Where to Find It

What a Waste

Full Disclosure

People, Their Pets and Pet Peeves

Parental Guidance

Aunt Evelyn's Letters

Most Popular Lessons

The HIV Life Cycle


Herpes Simplex Virus

Syphilis & Neurosyphilis

Treatments for Opportunistic Infections (OIs)

What is AIDS & HIV?

Hepatitis & HIV

email print

March 1999

HIV’s Incredible Endgame

by Lark Lands

Cult members stood up by an alien spaceship aren’t the only adherents of mass suicide. New research suggests that the strain of HIV—called syncytium-inducing (SI)—common in late-stage disease may prompt CD8 cells (key virus suppressors) to destroy themselves, a process known as apoptosis. This cellular suicide is a normal mechanism used by the body to eliminate damaged or cancerous cells. But researchers at the University of California at San Francisco and the Picower Institute for Medical Research at New York’s North Shore University Hospital report that when the SI virus binds to a surface protein called CXCR4—found on both CD8 cells and macrophages (microbe-scavenging cells)—the result is massive destruction of healthy CD8s. They believe that this might help explain why many PWAs experience a sudden, sharp slide toward illness after years of relative health.

The strategy the virus uses is notably different from the way it commandeers the CD4 cell. Instead of infiltrating and taking over its machinery, the virus’ binding to CXCR4 appears to be interpreted by the CD8 as a death signal. The mechanism that waves the white flag and triggers apoptosis is likely a cell-produced chemical called tumor necrosis factor-alpha (TNF-alpha). The researchers report that this mass apoptosis only occurs when macrophages are present, and that both they and the CD8 cells produce TNF-alpha. The result is a steep decline in CD8 cells, and therefore a decreased control of HIV. In turn, this results in greater vulnerability to opportunistic infections.

Although limited to test-tube studies so far, the researchers believe that this new understanding may lead to new avenues of therapy. Eric Verdin of UCSF says, “Right now, everyone’s focused on finding ways to block CCR5,” the molecule that allows cells to become infected by the non-syncytium-inducing, early-stage HIV. “Our research shows that it may be just as important to find ways to stop viruses that bind to CXCR4.”

[Go to top]

Facebook Twitter Google+ MySpace YouTube Tumblr Flickr Instagram
Quick Links
Current Issue

HIV Testing
Safer Sex
Find a Date
Newly Diagnosed
HIV 101
Disclosing Your Status
Starting Treatment
Help Paying for Meds
Search for the Cure
POZ Stories
POZ Opinion
POZ Exclusives
Read the Blogs
Visit the Forums
Job Listings
Events Calendar
POZ on Twitter

Ask POZ Pharmacist

Talk to Us
Has a pet helped you deal with your HIV?


more surveys
Contact Us
We welcome your comments!
[ about Smart + Strong | about POZ | POZ advisory board | partner links | advertising policy | advertise/contact us | site map]
© 2016 Smart + Strong. All Rights Reserved. Terms of use and Your privacy.
Smart + Strong® is a registered trademark of CDM Publishing, LLC.