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Comment: Most of these sources are inaccessible to me - adding accessible sources will help the review process. However, I note a number of unsourced statements relating to personal life. See WP:BLP. Statements, starting with the date of birth, need to be sourced or removed. Greenman (talk) 10:06, 29 November 2024 (UTC)
Eva Maria Fenyö (born Padányi Éva, on March 18 1940 in Budapest, Hungary) is a Hungarian-Swedish scientist. She began her medical studies in 1960 at the Semmelweis University in Budapest, but her career choices were constrained by the political situation in Hungary.[1] and she moved to Sweden in 1965 where she engaged in research at the Department of Tumor Biology, Karolinska Institute (KI), under the supervision of George and Eva Klein. Focusing on research, she continued her medical studies and obtained a PhD in 1974 in tumor biology and an MD in 1975 from KI. In 1981 Fenyö became a lecturer in virology and in 1997 a professor at the Karolinska Institute, Stockholm. In 1999 she became professor of virology at the Medical Faculty of Lund University, Lund, Sweden. In 2001 she became an elected member of the Royal Physiographic Society in Lund.
Fenyö’s research focused on retrovirus-host cell interactions. She transferred her experience from the mouse leukemia virus field[2] to human and simian immunodeficiency viruses (HIV and SIV) and enabled the formulation of two basic concepts for HIV/AIDS. One concept concerned HIV biological variability[3][4][5] that governs the virus ability to infect different cells and is tightly linked with the severity of infection[6]. The other concept concerned emergence of neutralisation resistant virus variants[7][8][9] that evade antibodies of the infected host.
Fenyö’s initial work addressed several aspects of HIV/AIDS. She found that HIV was present in the cerebrospinal fluid of HIV infected people[10] and pioneered the field of mother-to-child transmission of HIV[11][12][13]. She explored the biological variability of the less pathogenic HIV-2[14][15] and showed that HIV-2 infection mitigates subsequent HIV-1 infection of the same host[16]
Fenyö carried out HIV vaccine research within the framework of several international networks. Long-lasting collaboration, initiated in 1989, was established with WHO (later WHO-UNAIDS). The WHO-UNAIDS Network for HIV Isolation and Characterization (coordinated by the WHO-UNAIDS HIV Vaccine Initiative) performed the first, systematic world-wide survey of HIV isolates[17][18]. Fenyö was responsible for the biological characterization of HIV isolates and the development of a Guideline for HIV Isolation and Characterization, published in 1994 and a revised and extended version in 2002[19]. The Guidelines were used in WHO-UNAIDS-sponsored training workshops, conducted by Fenyö, for HIV biological and immunological characterization on potential vaccine trial sites (Stockholm 2000, Abidjan 2002, Rio de Janeiro 2003).
Fenyö participated in several European HIV vaccine research networks. HIV Variability (coordinator 1994-1997), NeutNet (2004), VIAV (2005-2007), EUROPRISE (2007-2011) and NGIN (2007-2012). She developed new techniques for HIV neutralisation[20][21]. Collaboration for AIDS Vaccine Discovery (CAVD), in support of the Global HIV Vaccine Enterprise, allowed the organization of three more training workshops (Sulzbach 2008, Cape Town 2009 and 2011).
She was married to Egon Fenyö from 1964 until his death in 2006. They had one son, David Fenyö, who is a professor at New York University Grossman School of Medicine focusing on computational biology research and education.
References
edit- ^ Eva Maria Fenyö: Kort gästspel på Horányikliniken (Swedish translation György Fenyö and Eva Dickson). chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/http://fenyo.se/documents/Horanyikliniken.pdf. Title of the Hungarian original: Rövid vendégszereplés a Horányi klinikán, A Mi Klinikánk: Emlékek a Balassa utcából, Semmelweis kiadó, 2012, 63-66.
- ^ Fenyö EM: Characteristics of mouse C-type viruses: Virus-host cell relations. Academic dissertation. Department of Tumor Biology, Karolinska Institute. Stockholm, 1974.
- ^ Åsjö B et al.: Replicative capacity of human immunodeficiency virus from patients with varying severity of HIV infection. Lancet ii, 660-662, 1986.
- ^ Fenyö EM et al.: Distinct replicative and cytopathic characteristics of human immunodeficiency virus isolates. J Virol 62:4414-4419, 1988.
- ^ Berger EA, Doms RW, Fenyö EM et al.: A new classification for HIV-1. Nature 391:240, 1998.
- ^ Fenyö EM, Esbjörnsson J, Medstrand P, Jansson M. Human immunodeficiency virus type 1 biological variation and coreceptor use: from concept to clinical significance. J Intern Med. 270:520-31, 2011.
- ^ Albert J et al.: Rapid development of isolate-specific neutralizing antibodies after primary HIV-1 infection and consequent emergence of virus variants which resist neutralization by autologous sera. AIDS 4:107-112, 1990.
- ^ Scarlatti G et al.: Mother-to-child transmission of HIV-1: Correlation with neutralising antibodies against primary isolates. J Inf Dis, 168:207-210, 1993.
- ^ Zhang Y-j et al.: Autologous neutralizing antibodies to SIVsm in cynomolgus monkeys correlate to prognosis. Virology 197, 609-615, 1993.
- ^ Chiodi F, Åsjö B, Fenyö EM et al.: Isolation of human immunodeficiency virus from cerebrospinal fluid of antibody-positive virus carrier without neurological symptoms. Letter Lancet ii, 1276-1277, 1986.
- ^ Scarlatti, G et al.: Comparison of V3 sequences from HIV-1 infected children to the RNA and DNA virus population of their mothers. Proc Natl Acad Sci, USA 90, 1721-1725, 1993.
- ^ Scarlatti G et al.: Evolution of viral coreceptor usage and sensitivity to chemokines during the progression of the disease in children infected with human immunodeficiency virus type 1. Nature Medicine 3:1259-1265, 1997.
- ^ Tscherning C et al.: The trophoblastic epithelial barrier is not infected in full-term placentae of human immunodeficiency virus-seropositive mothers undergoing antiretroviral therapy. J Virol. 73:9673-9678, 1999.
- ^ Albert J, Böttiger B, Biberfeld G and Fenyö EM: Replicative and cytopathic characteristics of HIV-2 and severity of infection. Lancet i:852-853, 1989.
- ^ Mörner A et al.: Primary HIV-2 isolates, like HIV-1, frequently use CCR5 but show promiscuity in coreceptor usage. J Virol. 73:2343-2349, 1999.
- ^ Esbjörnsson J,: Inhibition of HIV-1 disease progression by contemporaneous HIV-2 infection. N Engl J Med. 367:224-32, 2012.
- ^ WHO Network for HIV Isolation and Characterization: Three publications in AIDS Res Hum Retroviruses vol 10; pp. 1327-1344, 1387-1400 and 1401-1408, 1994.
- ^ Weber J, Fenyö EM et al.: Neutralisation serotypes of HIV-1 field isolates are not predicted by genetic subtype. J Virol 70:7827-7832, 1996.
- ^ chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/http://fenyo.se/documents/WHO-Guidelines-2002.pdf
- ^ Shi Y, Albert J, Francis G, Holmes H, Fenyö EM. A new cell line-based neutralization assay for primary HIV type 1 isolates. AIDS Res Hum Retroviruses. 18:957-67, 2002.
- ^ Sheik-Khalil E et al.: Automated image-based assay for evaluation of HIV neutralization and cell-to-cell fusion inhibition. BMC Infect Dis. 14:472, 2014. PMID:25176034.