In general, ebolavirions are 80 nanometers (nm) in width and may be as long as 14,000 nm.Their life cycle is thought to begin with a virion attaching to specific cell-surface receptors such as C-type lectins, DC-SIGN, or integrins, which is followed by fusion of the viral envelope with cellular membranes. The virions taken up by the cell then travel to acidic endosomes and lysosomes where the viral envelope glycoprotein GP is cleaved. This processing appears to allow the virus to bind to cellular proteins enabling it to fuse with internal cellular membranes and release the viral nucleocapsid. The Ebolavirus structural glycoprotein (known as GP1,2) is responsible for the virus ability to bind to and infect targeted cells. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. The most abundant protein produced is the nucleoprotein, whose concentration in the host cell determines when L switches from gene transcription to genome replication. Replication of the viral genome results in full-length, positive-strand antigenomes that are, in turn, transcribed into genome copies of negative-strand virus progeny. Newly synthesised structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane from which they bud. The mature progeny particles then infect other cells to repeat the cycle. The genetics of the Ebola virus are difficult to study because of EBOVs virulent characteristics.
Dens evaginatus is a rare odontogenic developmental anomaly that is found in teeth where the outer surface appears to form an extra bump or cusp. Premolars are more likely to be affected than any other tooth. It could occur unilaterally or bilaterally. Dens evaginatus (DE) typically occurs bilaterally and symmetrically. This may be seen more frequently in Asians (including Chinese, Malay, Thai, Japanese, Filipino and Indian populations).The prevalence of DE ranges from 0.06% to 7.7% depending on the race. It is more common in men than in women, more frequent in the mandibular teeth than the maxillary teeth. Patients with Ellis-van Creveld syndrome, incontinentia pigmenti achromians, Mohr syndrome, Rubinstein-Taybi syndrome and Sturge Weber syndrome are at a higher risk of having DE. Signs and symptoms
It is important to diagnose DE early and provide appropriate treatment to help prevent periodontal disease, caries, pulpal complications and malocclusion. It occurs on the cingulum/occlusal surface of the teeth. The extra cusp can cause occlusal interference, displace of the affected tooth and/or opposing teeth, irritates the tongue when speaking and eating and decay the developmental grooves. Temporomandibular joint pain could be experienced secondarily due to occlusal trauma caused by the tubercle.This cusp could be worn away or fractured easily. In 70% of the cases, the fine pulpal extension were exposed which can lead to infection, pulpal necrosis and periapical pathosis. Associated anomalies
Additional tubercules
Aesthetic and/or occlusion problems
Agenesis
Bifid cingula
Exaggerated cusp of Carabelli
Gemination
Impaction
Labial drifting
Labial groove
Mesiodens
Megadont
Odontoma
Peg-shaped lateral incisor
Prominent marginal ridge
Shallow groove in the lateral incisor
Shovel-shaped incisor
Supernumerary

Cause
The cause of DE is still unclear.