It is, therefore, a defective virus and cannot replicate without the help of hepatitis B virus.

And if defective viruses do not account for long-term non-progressors, then such individuals presumably must mount a phenomenal immune response.

In this experiment and in the clinical trials, the defective viruses are injected directly into the tumor.

Occasionally errors occur in the replicative cycle of a virus and defective viruses begin to appear in cells.

Studies elsewhere have shown that the delta virus is a defective virus that seems incapable of causing illness by itself.

But the defective virus could replicate in tumor cells that had disabled their own p53, and go on to attack other tumor cells.

In preclinical studies, the company reported that the defective virus killed laboratory cultures of p53-deficient tumor cells but was harmless to normal cells.

These defective viruses have usually lost a portion of their genetic material or suffered a single mutation that prevents them completing the full replicative cycle.

In other words, the defective virus was in principle the long-sought agent that could discriminate between normal and cancerous cells, killing only the latter.

Viruses are error-prone as they multiply, producing an array of defective viruses, most of which are incapable of further propagation.

Scientists are trying to determine whether lack of progression in such people - often called long-term nonprogressors - is due to an unknown factor in their immune systems or to a defective virus.

A novel form of cancer treatment, based on a defective virus that can grow only in cancerous cells, has passed another milestone by showing promise in treating patients with recurrent head and neck cancer.

In vitro studies have shown that lymphocyte infection produces tumor cell populations comprising three types of cells: stable productive cells, non-productive cells and cells which produced defective virus particles which are not infective.