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West Nile Virus: Keep Calm and Carry Bug Repellant

, by Reilly O'Neal

West Nile virus (WNV) is an infection spread primarily through mosquito bites. The first known U.S. case was reported in 1999; since then, upwards of 30,000 cases have been reported nationwide, according to the U.S. Centers for Disease control and Prevention (CDC).

As of September 4, 2012, a total of 1,993 cases of WNV have been reported in the United States—a record-breaking number for this time of year, leading to speculation that the 2012 outbreak will be the country’s worst yet. Eighty-four people have died from West Nile disease this year.

(While these figures are both alarming and sobering, it’s important to keep the West Nile virus outbreak in perspective: As noted in an August 25 New York Times editorial, a typical flu season sees 25,000 to 36,000 deaths.)

Are people with HIV at greater risk for West Nile virus? How can infection be avoided? And what’s next for someone who may have been exposed? Read on for answers.

Are HIV-Positive People at Higher Risk from WNV?

The short answer is “yes.” The CDC warns that people with compromised immune systems and those over age 50 are at greatest risk for developing severe West Nile virus disease. Given their already burdened immune systems, people with HIV may become more seriously ill if infected with West Nile virus.

In addition, neurologist Gregory Pauxtis, MD, of California Pacific Medical Center in San Francisco says the CDC’s warning about older adults has less to do with chronological age than with immune system health. As we age, we experience “immunosenescence,” marked by a gradual decline in production of T cells—key players in the body’s response to infection—and weakened immune response. Studies have detected earlier immunosenescence in people with HIV, suggesting that their already strained immune systems may put them at greater risk for complications of West Nile virus.

(Regardless of your HIV status, you can prevent serious illness from West Nile virus by avoiding exposure in the first place. See below for tips on staying WNV-free.)

How Serious is West Nile Disease?

Not everyone with West Nile virus infection ever feels sick: The CDC estimates that roughly 80% of people clear the infection with no symptoms at all. Those who do have disease symptoms may experience fever, headache and body aches, nausea or vomiting, possibly swollen lymph glands, or a rash on the chest, stomach, and back. These symptoms can last just a few days or up to several weeks.

A small proportion—about one in 150, according to the CDC—develop severe illness. Symptoms may include high fever, neck stiffness, headache, stupor or disorientation, tremors or convulsions, muscle weakness, loss of vision, numbness, and even paralysis or coma.

These more severe symptoms can last several weeks and stem from “neuroinvasive” disease that has affected the nervous system—the network of nerves and specialized cells that relay “messages” between the brain and every organ in the body. The effects of neuroinvasive disease may be permanent and life-altering.

CCR5, Maraviroc, and West Nile Virus

“On the neuroinvasive side, we have never really understood why some people become ill and some people don’t” in the general population, said Dr. Pauxtis. However, one clue comes from reports linking a rare genetic mutation with more severe cases of West Nile virus.

Worldwide, an estimated 1% of people of European ancestry carry the CCR5-delta-32 mutation, which renders an individual’s CD4 cells—key cells in the immune system—unable to properly produce a protein called CCR5. This mutation is important in HIV research today, because the CCR5 protein serves as a “co-receptor” that allows HIV to enter and infect CD4 cells. People whose cells do not make CCR5 are essentially resistant to HIV infection.

However, carriers of the mutation, while protected against HIV, appear to be at higher risk for complications from WNV. A 2008 meta-analysis of data from Caucasians with severe West Nile disease in four states (Arizona, California, Colorado, and Illinois) found that 4.2% had the CCR5-delta-32 mutation—far higher than the estimated 1% of whites with the mutation in the U.S.

A later study published in 2010 found no link between the CCR5-delta-32 mutation and risk for becoming infected with West Nile virus, suggesting that lack of CCR5 does not increase risk for merely acquiring the virus. However, the researchers noted that the mutation “was associated with worse clinical outcome, with these individuals developing more clinical symptoms.”

While the CCR5-delta-32 mutation is fairly uncommon, concern over the link between sever WNV illness and the mutation reaches beyond this population: People who have their CCR5 blocked or “deleted” as part of HIV therapy.

The HIV drug maraviroc (Selzentry) is a CCR5 “antagonist” that effectively mimics the CCR5-delta-32 genetic mutation by attaching to the CCR5 co-receptor so HIV can’t use it to enter cells. Two experimental therapies—genetic modification of HIV-positive individuals’ cells to lack CCR5, and the bone marrow stem cell transplants that appear to have cured one man, “Berlin Patient” Timothy Brown of HIV infection—are also modeled on the CCR5-delta-32 mutation. These procedures aim to replace HIV-infected immune system cells with cells from donors who carry the CCR5-delta-32 mutation, in the hope of inducing an HIV-resistant immune system.

These approaches herald an exciting new era in HIV treatment and cure research. But could the lack of the CCR5 protein, induced in the lab or the clinic, put people at greater risk for serious illness from West Nile virus?

“It makes sense—although not borne out in statistics—that blocking [CCR5] with the medication will also increase West Nile virus virulence,” said Dr. Gregory Pauxtis, speaking about the CCR5 antagonist drug maraviroc. But to date, no data or anecdotal observations have been reported linking West Nile disease with maraviroc use, gene therapy trials for HIV treatment, or the stem cell transplants completed by Timothy Brown.

As users of these relatively new therapies are followed over time, new data may shed light on their risk for more severe West Nile disease—or their lack of it.

Preventing Exposure to West Nile Virus

As mentioned above, West Nile virus spreads primarily through bites from infected mosquitoes, although a small number of documented transmissions have occurred through blood transfusions, organ transplants, and from mother to infant during pregnancy or breastfeeding.

To protect yourself against West Nile virus, consider the following precautions recommended by the CDC:

  • Prevent mosquito bites. 
    • When you’re outdoors—especially at dusk and dawn, when mosquitoes are most active—use insect repellent containing the CDC-recommended ingredients DEET, picaridin, oil of lemon eucalyptus or PMD, or IR3535. (If you have sensitive skin, talk with your medical provider or pharmacist first to learn whether these repellents or an alternative product would be appropriate for you.)
    • Use screens (and repair torn ones) on your windows and doors to keep mosquitoes out of your home.
    • Mosquitoes breed in standing water. Cut down their population by emptying water from flower pots, buckets, barrels, and by changing the water in pet dishes and bird baths weekly. Visit the CDC’s “Fight the Bite!” page for more tips on eliminating standing water.
  • Drop that bird! In addition to counting human cases, public health agencies track numbers of dead birds that test positive for WNV, because mosquitoes pick up the virus from infected birds. Although there are no known cases of WNV transmission from handling a dead bird, the California Department of Public Health’s West Nile virus website recommends not handling dead birds with your bare hands. You can report dead birds to your local public health department.

If You Think You’ve Got WNV

The incubation period—the time from infection with the virus to the beginning of symptoms—for West Nile disease is usually 2 to 15 days. If you were bitten by a mosquito and later experience symptoms or otherwise suspect you may have WNV, your medical provider can run a blood test for the presence of antibodies to the virus or for RNA, the virus’ genetic material. Other procedures, including lumbar puncture (spinal tap) or brain imaging (EEG or MRI), may be performed to confirm neuroinvasive West Nile disease.

While there is no direct-acting treatment or cure, supportive therapies can help resolve symptoms and prevent other infections from taking hold while the body recovers. These may include over-the-counter pain medications, intravenous fluids, and other medications given in a hospital setting.

Conclusion

While this year’s West Nile outbreak may turn into the nation’s worst yet, WNV still kills far fewer people each year than does plain old flu. Indeed, the number of deaths due to influenza each year is 19 to 27 times higher than the total number of West Nile deaths in the U.S. since 1999.

Still nervous? Click here for the CDC’s surveillance map and see whether WNV cases have been reported in your area. But keep in mind that, while people with HIV may be at greater risk for developing severe illness from West Nile virus infection, basic precautions against mosquito bites can protect everyone, regardless of their HIV status or immune health. And good communication with your medical team can help rule out or confirm WNV infection and get you started on any supportive therapies, ease symptoms, and safeguard your health.

Reilly O’Neal is a freelance writer and former editor of BETA.

Sources

CDC. “Fight the Bite!” http://www.cdc.gov/ncidod/dvbid/westnile/index.htm

Deeks, S. HIV infection, inflammation, immunosenescence, and aging. Annual Review of Medicine 62:141–55. February 18, 2011.

Glass, W. CCR5 deficiency increases risk of symptomatic West Nile virus infection. Journal of Experimental Medicine 203(1):35–40. January 23, 2006.

Lim, J. and others. CCR5 deficiency is a risk factor for early clinical manifestations of West Nile Virus infection, but not for infection per se. Journal of Infectious Diseases 201(2):178–85. January 15, 2010.

Lim, J. and others. Genetic Deficiency of chemokine receptor CCR5 is a strong risk factor for symptomatic West Nile virus infection: A meta-analysis of 4 cohorts in the US epidemic. Journal of Infectious Diseases 197(2):262–65. January 15, 2008.

 

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