This collaborative effort also involved researchers from Institute of Biomedical Research and the United States Army Medical Research Institute of Infectious Diseases. A survivor from the 1995 outbreak of Ebola virus disease in Kikwit, Democratic Republic of Congo donated blood to the project that began roughly ten years after they had recovered. Memory B cells isolated from the survivors blood were immortalized, cultured and screened for their ability to produce monoclonal antibodies that reacted with the glycoprotein of Ebola virus. Ansuvimab was identified from one of these cultures and the antibody heavy and light chain gene sequences were sequenced from the cells. These sequences were then cloned into recombinant DNA plasmids  and purified antibody protein for initial studies was produced in cells derived from HEK 293 cells. Ansuvimab and mAb100 combination
In an experiment described in the 2016 paper, rhesus macaques were infected with Ebola virus and treated with a combination of ansuvimab and another antibody isolated from the same subject, mAb100. Three doses of the combination were given once a day starting 1 day after the animals were infected. The control animal died and the treated animals all survived. Ansuvimab monotherapy
In a second experiment described in the 2016 paper, rhesus macaques were infected with Ebola virus and only treated with ansuvimab. Three doses of ansuvimab were given once a day starting 1 day or 5 days after the animals were infected. The control animals died and the treated animals all survived.
Tay syndrome should not be confused with the Tay–Sachs disease. : 485   It is an autosomal recessive congenital disease. : 501  In some cases, it can be diagnosed prenatally. IBIDS syndrome is nonphotosensitive. Cause
The photosensitive form is referred to as PIBIDS, and is associated with ERCC2 and ERCC3. Photosensitive forms
All photosensitive TTD syndromes have defects in the nucleotide excision repair (NER) pathway, which is a vital DNA repair system that removes many kinds of DNA lesions. This defect is not present in the nonphotosensitive TTDs. These type of defects can result in other rare autosomal recessive diseases like xeroderma pigmentosum and Cockayne syndrome. DNA repair
Currently, mutations in four genes are recognized as causing the TTD phenotype, namely TTDN1, XPB, XPD and TTDA. Individuals with defects in XPB, XPD and TTDA are photosensitive, whereas those with a defect in TTDN1 are not. The three genes, XPB, XPD and TTDA, encode protein components of the multi-subunit transcription/repair factor IIH (TFIIH). This complex factor is an important decision maker in NER that opens the DNA double helix after damage is initially recognized. NER is a multi-step pathway that removes a variety of different DNA damages that alter normal base pairing, including both UV-induced damages and bulky chemical adducts. Features of premature aging often occur in individuals with mutational defects in genes specifying protein components of the NER pathway, including those with TTD (see DNA damage theory of aging). Diagnosis
Treatment
See also
Skin lesion
List of cutaneous conditions

References
External links
NIH document on Tay syndrome