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A 1959 promotion of the Veterinary School at MaisonsAlfort (Gérard Orth is indicated by the red cross). B 1959-1960 promotion of the Microbiology cours at Pasteur Institute (Gérard Orth is indicated by the red arrow)
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Context 1
... He later admitted that this was "an aberration for him and his parents". He suffered two years of intense study at the Lycée Marcelin Berthelot in Saint Maur des Fossés. Marcelin Berthelot was a nineteenth century French chemist and polymath. Gérard then attended the national veterinary school at MaisonsAlfort near Paris between 1955 and 1959 ( Fig. 1A). Gérard had only a few friends among his classmates at Maisons-Alfort, one of the most important of whom was Jean-Charles Friedmann, to whom he owed his admiration for Charles de Gaulle and unreserved support for the General's actions after his return to power. Gérard recalled that "Charles de Gaulle was a mentor for me. He instilled ...
Context 2
... He admired many, and perhaps especially Gaston Ramon , who had discovered the principle of vaccination with anatoxin. Gérard attended the Microbiology (1960) and Immunology (1960) courses at the Institut Pasteur in Paris. The "Grand Cours de Microbiologie", now defunct, was the heir to the "Cours de Microbie Technique" created by Pasteur in 1889 (Fig. 1B). Its primary purpose was to teach systematic microbiology. However, it also represented an opportunity, then unique in France, to discover the nascent molecular microbiology developed at the Institut Pasteur by André Lwoff, Jacques Monod, François Jacob, and Elie Wollman. Gérard had bought and read with great interest "The sexuality of ...
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... Genetic diagnosis was facilitated by using a gene list for IEIs developed by the Expert Committee of the International Union of Immunological Societies (IUIS). β-HPVs were amplified from DNA extracted from the lesion swab, as previously described [12]. Sanger sequencing was used to confirm the genotypes of β-HPVs and the STK4 variant. ...
The clinical penetrance of infectious diseases varies considerably among patients with inborn errors of immunity (IEI), even for identical genetic defects. This variability is influenced by pathogen exposure, healthcare access and host-environment interactions. We describe here a patient in his thirties who presented with epidermodysplasia verruciformis (EV) due to infection with a weakly virulent beta-papillomavirus (HPV38) and CD4 ⁺ T-cell lymphopenia. The patient was born to consanguineous parents living in the United States. Exome sequencing identified a previously unknown biallelic STK4 stop-gain mutation (p.Trp425X). The patient had no relevant history of infectious disease during childhood other than mild wart-like lesion on the skin, but he developed diffuse large B-cell lymphoma (DLBCL) and EBV viremia with a low viral load in his thirties. Despite his low CD4 ⁺ T-cell count, the patient had normal counts of CD3 ⁺ cells, predominantly double-negative T cells (67.4%), which turned out to be Vδ2 ⁺ γδ T cells. γδ T-cell expansion has frequently been observed in the 33 reported cases with STK4 deficiency. The Vδ2 γδ T cells of this STK4-deficient patient are mostly CD45RA ⁻ CD27 ⁺ CCR7 ⁺ central memory γδT cells, and their ability to proliferate in response to T-cell activation was impaired, as was that of CD4 ⁺ T cells. In conclusion, γδ T-cell expansion may act as a compensatory mechanism to combat viral infection, providing immune protection in immunocompromised individuals.
