T280M Variation of the CX3C Receptor Gene Is Associated With Increased Risk for Severe Respiratory Syncytial Virus Bronchiolitis

Amanatidou, Virginia; Sourvinos, George; Apostolakis, Stavros; Tsilimigaki, Amalia; Spandidos, Demetrios Α.

doi:10.1097/01.inf.0000214998.16248.b7

Cited by 52 publications

(39 citation statements)

References 32 publications

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“…Recent studies have demonstrated that inflammatory mediators play essential roles in enhancing respiratory viral pathologies [15][16][17][18][19]; however, several of these mediators have not yet been identified. The contribution of host immune responses to the pathologies observed during respiratory viral infections opens up the potential for therapeutic alternatives based on the suppression of pathogenic immune response.…”

Section: Introductionmentioning

confidence: 99%

Distinctive and critical roles for cellular immunity and immune-inflammatory response in the immunopathology of Sendai virus infection in mice

Simon

Sasaki

Ichii

et al. 2011

Microbes and Infection

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Overall, DBA/2J mice exhibited a dysregulated hyper-inflammatory cytokine/chemokine cascades that does not limit viral spread resulting in a predisposition to severe lung pathology. This response is similar to severe human respiratory paramyxovirus infections, which will serve as a model for the elucidation of hyper-immune inflammatory response that result to severe immunopathology in respiratory viral infections.

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Section: Introductionmentioning

confidence: 99%

Distinctive and critical roles for cellular immunity and immune-inflammatory response in the immunopathology of Sendai virus infection in mice

Simon

Sasaki

Ichii

et al. 2011

Microbes and Infection

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“…For example, CX3CR1 polymorphisms have been implicated in conditions such as Crohn's disease, multiple sclerosis, and bronchiolitis among Caucasians [25][26][27]. Further downplaying the possible role of CX3CR1 genetic polymorphism on HIV infection, no significant differences in CX3CR1 745G>A genotype and allele frequencies between HIV EI and EU children were observed (Table 3).…”

Section: Chemokine Receptor Polymorphism and Their Association With Hmentioning

confidence: 84%

CCR2, CX3CR1, RANTES and SDF1 genetic polymorphisms influence HIV infection in a Zimbabwean pediatric population

Mhandire

Duri

Kandawasvika

et al. 2014

J Infect Dev Ctries

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Introduction: There is growing evidence that polymorphisms in chemokine and chemokine receptor genes influence susceptibility to HIV infection and disease progression. However, not much is documented about the prevalence and effects of chemokine and chemokine receptor gene variations in the Zimbabwean population despite the high burden of HIV/AIDS in the country. This study therefore describes polymorphisms in CCR2, CX3CR1, SDF1 and RANTES genes in a Zimbabwean pediatric population and their effects on HIV infection in children born to HIV-infected mothers. Methodology: A total of 106 children between seven and nine years of age comprising 70 perinatally exposed to HIV (34 born infected [EI] and 36 born uninfected [EU]) and 36 unexposed and uninfected (UEUI) controls were recruited. Six allelic variants in four genes were genotyped using PCR-RFLP and sequencing. Results: Frequencies for minor alleles in the HIV uninfected groups (EU and UEUI) were CCR2 190A (16%), SDF1 801A (2%), CX3CR1 745A (9%), CX3CR1 839T (0%), RANTES In 1.1C (20%), and RANTES -403A (44%). There were significant differences between the EI and EU groups in the distribution of CCR2 190G/A genotype (15% versus 39%, respectively, p = 0.02) and CCR2 190G/A-CX3CR1 745G/G genotype combination (0% versus 33%, respectively, p = 0.002). Conclusions: Our findings suggest that chemokine and chemokine receptor gene variants seem to play an important role in the dynamics of HIV infection and could be used as drug or vaccine targets.

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“…'lar›, CX 3 CR1 Thr280Met SNP'de fliddetli RSV bronfliyolit riskinin artm›fl oldu¤unu göstermifllerdir. Bu mutasyon, hem virüslerin giriflini kolaylaflt›rarak, hem de viral klirens etkinli¤ini azaltarak uygunsuz uyar› ve immünopato-jenik immün yan›ta neden olmaktad›r (47).…”

Section: Akut Bronfliyolitte Immün Yan›t Ve Doku Hasar› Iliflkisiunclassified

Çocukluk çağında bronşiyolitler: Etiopatojenez ve immünolojik akciğer hasarındaki yenilikler

Yüksel¹,

Türkeli²,

Yılmaz³

et al. 2011

tpa

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Ç Ço oc cu uk kl lu uk k ç ça a¤ ¤› ›n nd da a b br ro on nfl fli iy yo ol li it tl le er r: : E Et ti io op pa at to oj je en ne ez z v ve e i im mm mü ün no ol lo oj ji ik k a ak kc ci i¤ ¤e er r h ha as sa ar r› ›n nd da ak ki i y ye en ni il li ik kl le er r B Br ro on nc ch hi io ol li it ti is s i in n c ch hi il ld dh ho oo od d: : U Up pd da at te es s o on n e et ti io op pa at th ho og ge en ne es si is s a an nd d i im mm mu un no ol lo og gi ic c l lu un ng g i in nj ju ur ry y GiriflAkut bronfliyolit, iki yafl›ndan küçük çocuklarda s›kl›kla viral etkenlerin neden oldu¤u bronfliyollerin enflamasyonuyla belirgin h›fl›lt› 'wheezing', öksürük, h›zl› solunum, gö-¤üste çekilmeler ve ekspiryumda uzama ile seyreden bir hastal›kt›r (1). S›k görülmesi, tekrarlayan tablolar›n›n ast›m ile olas› iliflkisi, süt çocuklu¤unda ciddi hastal›k ve ölüm nedeni oluflturmas› hastal›¤›n önemini artt›rmaktad›r (2).Ancak enfeksiyon etkenleriyle karfl›laflan çocuklar›n tamam›nda alt solunum yolu enfeksiyonu geliflmemektedir. Enfeksiyona yatk›nl›k ve bronfliyolitin klinik olarak fliddetli seyretmesinde kona¤›n havayolundaki immünolojik, yap›-sal ve ifllevsel özellikleri önem tafl›maktad›r (3). Patojenlerin bronfl alan›na ulaflmalar›ndan sonra birincil hedefleri olan epitel hücrelerinde oluflan enflamasyona (virüsün virülans›, immünolojik yan›t) ba¤l› olarak bronfliyolitin klinik tablodaki a¤›rl›¤› de¤iflkenlik göstermektedir (4). Bunlar›n yan›nda S Su um mm ma ar ry yAcute bronchiolitis is a disease characterized with bronchiolar inflammation due to viral infections in children younger than two years that is associated with wheezing, cough, tachypnea, retractions and prolonged expiration. Many pathogens, among which respiratory syncytial virus is the most common, play role in the etiology. Cellular damage due to viral pathogens and anatomic and immunological factors of the host play a role in the development of lower respiratory tract infections only in some children exposed to respiratory syncytial virus and other viruses. Viral infections in children may change Th1/Th2 immune response pattern. Severity of disease changes with the degree of inflammation due to the immune response. Moreover, an increase in disease severity may be observed due to the activation of the nonadrenergic non-cholinergic neurogenic system. Severe RSV infections may develop in children with genetic predisposition. We explained the role of environmental factors, genetic and structural susceptibility of the host, and contribution of immunologic response in this susceptibility, in addition to the role of responsible infectious agents, in the development and severe progression of bronchiolitis (Turk Arch Ped 2010; 45: 75-81)

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T280M Variation of the CX3C Receptor Gene Is Associated With Increased Risk for Severe Respiratory Syncytial Virus Bronchiolitis

Abstract: Our findings support the hypothesis of the pivotal role of the G glycoprotein CX3CR1 pathway in the pathogenesis of RSV bronchiolitis and propose CX3CR1 as a potential therapeutic target.

Cited by 52 publications

References 32 publications

Distinctive and critical roles for cellular immunity and immune-inflammatory response in the immunopathology of Sendai virus infection in mice

Distinctive and critical roles for cellular immunity and immune-inflammatory response in the immunopathology of Sendai virus infection in mice

CCR2, CX3CR1, RANTES and SDF1 genetic polymorphisms influence HIV infection in a Zimbabwean pediatric population

Çocukluk çağında bronşiyolitler: Etiopatojenez ve immünolojik akciğer hasarındaki yenilikler

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