Government scientists have shown that a virus infection can cause diabetes, and the discovery could lead to a vaccine to prevent some of the disease's worst cases.

The form of diabetes involved is "juvenile-onset," or insulin-dependent, diabetes. This is a different disease and a farm more serious one than the milder adult-onset didbetes that generally can be controlled by diet or drugs.

In the last five years, scientists increasingly believed that any one of several viruses, as well as other causes, could trigger juvenile-onset diabetes in susceptible persons.

Now, researchers at the National Institutes of Health and the National Naval Medical Center in Bethesda for the first time have isolated a plainly guilty virus-one from a 10-year-odl suburban Maryland boy who developed juvenile-onset diabetes and died within weeks.

The doctors who reported the isolation of this Coxsackie B4 virus, a ubiquitous bug that is commonly responsible for many cold-like symptons, are NIH Drs. Ji-Won Yoon, Takashi Onodera and Abner Louis Notkins, and Dr. Marshall Austin of the Naval Medical Center.

In today's issue of the New England Journal of Medicine, these doctors and scientists say the Coxsackie virus -and other kinds of viruses, too-may infect hundreds of persons with little or no effect, but that the occasional susceptible person develops diabetes.

In an editorial in the same issue, Dr. Allan Drash of Pittsburg Children's Hospital credits the NIH-Naval Center team with finally "docmenting"-or proving -that juvenile-onset diabetes can result from a virus infection.

With other new insights, says Drash, this "highly important" achievement could eventually lead to several further advances. These could include identification of some susceptible persons and immunization of some with a preventive vaccine, as well as development of drugs that could block the disease's worst effects-effects that can sometimes include early or eventual blindness, loss of limbs and heart disease, as well as death.

The NIH and Navy men and Dr. Drash all emphasize that science still must learn exactly which viruses may causes diabetes and whether their role is more or less important than other possible "triggers": environmental poisons and chemicals, for example.

These accidents think there may be many possible causes of juvenile-onset diabetes. They think the disease may develop only in genetically susceptible individuals. They think there may also have to be a breakdown in the body's disease-fighting system.

Still, said Drash, observation of many patients suggests that juvenile-onset diabetes sometimes follows Coxshackie B4 infections "by weeks," mumps infections "by months to several years," and even exposure of a fetus in the womb to its mother's German measles "by as much as 15 to 20 years."

One child or younger person in 1,000 develops this form of diabetes, according to the Juvenile Disease Foundation. Among the 10 million diabetics in America, there are 1.5 million with the disease.

The federal virus work was done in NIH's National Institute of Dental Research as part of that Institute's general interest in glands of secretion. Diabetes is a disorder of the pancreas gland, the secretor of natural insulin.

Only last year Notkins, Yoon and Onodera proved that two common human viruses - the Coxsackie and a "reo type 3" virus, one that often causes respiratory and intestinal disease-could trigger diabetes in susceptible mice.

Early last year Dr. Austin, a naval hospital M.D. and pathologist and Ph. D. in virology, was assigned to conduct an autopsy on the boy, 10, who had just died there of his sudden diabetes.

Austin-who knew of the NIH group partly because his virology teacher at Duke University had been Dr. Notkins' student-immediately phoned the NIH people, just across Rockville Pike from the naval institution. He told them he had taken essential pancreas and other tissue samples from the boy.

Yoon and colleagues then isolated the Coxsackie virus from the child's diabetes-ridden pancreas cells. They successfully grow it in cultures of both animal and human cells.

They then injected it into genetically diabetes-prone mice and caused the pancreas damage and other symptons typical of diabetes. They then recovered the same virus from the infected animals.

By these four essential steps, Dr. Drash points out, the NIH scientists had fulfilled Koch's four classic postulates-the rules laid down by the famed German bacteriologist, Robert Koch, for proving that a microscopic organism is a disease's cause.