When Did AIDS Begin? How?

When Did AIDS

Begin?

Reprinted from Times Magazine, By Christine Gorman

Spring 1988

A new study of the oldest known HIV suggests the virus jumped from animals to humans in the 1940s.

The year was 1959, location: The central African city of Leopoldville, now called Kinshasa, shortly before the waves of violent rebellion that followed the liberation of the Belgian Congo. A seemingly healthy man walked into a hospital clinic to give blood for a Western backed study of blood diseases. He walked away and was never heard from again. Doctors analyzed his sample, froze it in a test tube and forgot about it. A quarter-century later, in the mid-1980s, researchers studying the growing AIDS epidemic took a second look at the blood and discovered that it contained HIV, the virus that causes AIDS.

And not just any HIV. The Leopoldville sample is the oldest specimen of the AIDS virus ever isolated and may now help solve the mystery of how and when the virus made the leap from animals (monkeys or chimpanzees) to humans, according to a report published last week in Nature. Dr. David Ho, director of the Aaron Diamond AIDS Research Center in New York City and one of the study's authors, says a careful genetic analysis of the sample's DNA pushes the origin of the AIDS epidemic back at least a decade, to the early '50s or even the '40s.

Over the past 15 years, scientists have identified at least 10 subtypes of the virus. But they couldn't tell whether they were seeing variations on one changeable virus or the handiwork of several different viruses that had made the jump from primates to man. A look at the genetic mutations in the Leopoldville sample strongly suggests that all it took to launch the epidemic was one unlucky turn of events.

By comparing the DNA of the 1959 virus with that of samples taken from the '80s and '90s. Ho and his colleagues constructed a viral family tree in which the Leopoldville isolate sits right at the juncture where three subtypes branch out. The 39-year-old specimen is also strikingly similar to the other seven subtypes. The clear implication: all the viral strains can be traced back to a single event or a closely related group of events. One theory is that AIDS started through contact with infected monkeys in a remote area and spread to the rest of the population through urbanization and mass inoculations.

The findings underscore how rapidly HIV can adapt to its surroundings, making it difficult to develop effective vaccines. No one knows how many more subtypes of HIV will sprout in the next 40 years, but chances are they will be every bit as lethal as the ones we see today, if not more so.

Apert Syndrome : A genetic disorder

Apert Syndrome


Introduction

Apert syndrome is a rare genetic disorder that is characterized by specific craniofacial and limb abnormalities. It is caused by a genetic mutation in the FGFR2 gene on chromosome 10. The mutation can be inherited from a parent who has Apert syndrome or it can be a spontaneous (new) mutation. Studies show that Apert syndrome tends to occur more often in children with older fathers. Furthermore, all new mutations (those that have not been inherited by an affected parent) have been shown to occur exclusively in the FGFR2 gene received by the father. Apert syndrome occurs in 1 out of 100,000 to 160,000 live births and affects males and females equally. The first reported case of the syndrome was in 1848 by S.W. Wheaton, and in 1906, a French physician named E. Apert described nine cases and defined the syndrome.

Features and Characteristics

The following characteristics have been found in children with Apert syndrome:

• Prematurely fused cranial sutures
• Retruded (or sunken) mid-face
• Fused fingers
• Fused toes
• Brachycephaly (short wide head)
• Acrocephaly (high prominent forehead)
• Flattened back of skull
• Prominent eyes - may be spaced widely apart or slant downward
• Strabismus
• Prominent mandible
• Depressed nasal bridge and small anteverted nose
• Down-turned corners of the mouth
• Low set ears (as well as hearing loss)
• Cleft palate
• Severe acne in teens
• Hydrocephalus
• Dental abnormalities (malposition of the teeth, crowding of the teeth, delayed tooth eruption, high-arched narrow palate, thickened ridges that support the teeth)
• Internal organ abnormalities including heart defects and abnormalities of the trachea,
  
• uterus, and brain

Skin manifestations of Apert syndrome

Hyperhidrosis Synonychia Brittle nails Severe acne in puberty Interruption of the eyebrows Hypopigmentation Hyperkeratosis Paronychial infections of plantar skin Excessive skin wrinkling of forehead Dimples at knuckles, shoulders and elbows

Prematurely Fused Cranial Sutures

Retruded Mid-face

Fused Fingers and Toes

Diagnosis

The diagnosis can be made by a skull x-ray, which will confirm premature closure of the skull, and by a clinical exam. The combination of the craniofacial problems and the fused fingers and toes is what distinguishes Apert syndrome from other similar syndromes. Since the defect which causes Apert syndrome has been identified, genetic testing can be provided to confirm a diagnosis.

Treatment

Treating a child with Apert syndrome is best accomplished with a team approach. This would include a craniofacial surgeon, neurosurgeon, ENT specialist, audiologist, speech pathologist, oral surgeon, psychologist, ophthalmologist, and an orthodontist. The majority of treatment methods is surgical and the individual will likely require many operations. Aside from the surgeries required to correct the craniofacial problems and the fused fingers and toes, there may be other potential surgeries to improve the upper airway, address severe eye problems, or correct dental issues.

A child with Cushing syndrome