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John McAfee, From Tech Pioneer to Murder Suspect

The bizarre events that have unfolded in recent days almost beggar belief: John McAfee, the tech entrepreneur who pioneered anti-virus software, has gone into hiding. He is a wanted man in Belize, the tiny Central American nation to which he retired in 2008.

McAfee, 67, had reportedly been tangling with Belizean authorities for months when his neighbor, fellow American expatriate Gregory Faull, was found murdered at home, shot once in the back of the head. Police immediately deemed McAfee a prime suspect and launched a manhunt for the eccentric fugitive.

A brief history of McAfee's unique life and career follows.

Related:The Most Bizarre and Dramatic Executive Blog You Might Ever Read

1987: McAfee, a former NASA programmer and private-sector software designer, founds McAfee Associates, a company designed to fix computer bugs. He decides to create the company after his computer is infected with the Pakistani Brain virus.

1989: McAfee leaves Lockheed, where he had been working, to focus full-time on his company.

He offers his VirusScan anti-virus program as shareware -- individuals and companies can download a free trial of the software, but must pay for licenses and continued use.

McAfee publishes a book, Computer Viruses, Worms, Data Diddlers, Killer Programs, and Other Threats to Your System.

August 1992: McAfee incorporates his company in Delaware, forming McAfee Associates Inc. At this time the company has 26 employees.

October 1992: The company goes public, selling 2.6 million shares and raising more than $40 million.

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John McAfee, From Tech Pioneer to Murder Suspect

Patient's own immune cells may blunt viral therapy for brain cancer

ScienceDaily (Nov. 25, 2012) Doctors now use cancer-killing viruses to treat some patients with lethal, fast-growing brain tumors. Clinical trials show that these therapeutic viruses are safe but less effective than expected.

A new study led by researchers at the Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James) shows that the reason for this is in part due to the patient's own immune system, which quickly works to eliminate the anticancer virus.

The findings, published in the journal Nature Medicine, show that the body responds to the anticancer virus as it does to an infection. Within hours, specialized immune cells called natural killer (NK) cells move in to eliminate the therapeutic virus in the brain.

The researchers discovered that the NK cells attack the viruses when they express specific molecules on their surface called NKp30 and NKp46. "These receptor molecules enable the NK cells to recognize and destroy the anticancer viruses before the viruses can destroy the tumor," says co-senior author Dr. Michael A. Caligiuri, director of Ohio State's Comprehensive Cancer Center and CEO of the James Cancer Hospital and Solove Research Institute, and a senior author of the study.

"When we blocked those receptors, the virus has more time to work, and mice with these brain tumors live longer. The next step is to block these molecules on NK cells in glioblastoma patients and see if we can improve their outcome," says Caligiuri, who is also the John L. Marakas Nationwide Insurance Enterprise Foundation Chair in Cancer Research. This study of cancer-cell-killing, or oncolytic, viruses is an example of the value of translational research, in which a problem observed during clinical trials is studied in the laboratory to devise a solution.

"In this case, clinical trials of oncolytic viruses proved safe for use in the brain, but we noticed substantial numbers of immune cells in brain tumors after treatment," says senior author and neurosurgeon Dr. E. Antonio Chiocca, who was professor and chair of neurological surgery while at Ohio State University.

"To understand this process, we went back to the laboratory and showed that NK cells rapidly infiltrate tumors in mice that have been treated with the therapeutic virus. These NK cells also signal other inflammatory cells to come in and destroy the cancer-killing virus in the tumor."

The study used an oncolytic herpes simplex virus, human glioblastoma tumor tissue and mouse models, one of which hosted both human glioblastoma cells and human NK cells. Key technical findings include:

"Once we identify the molecules on glioblastoma cells that these NK cell receptors bind with, we might be able to use them to identify patients who will be sensitive to this therapy," Caligiuri says.

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Patient's own immune cells may blunt viral therapy for brain cancer

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