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Shared biology of GVHD and GVT effects: Potential methods of separation: Critical Reviews in Oncology/Hemat ology, Vol. 57, No. 3. (March 2006), pp. 225-244.The difficult separation of clinical graft-versus-t umor (GVT) effects from graft-versus-h ost disease (GVHD) reflects their shared biology. Experimental approaches to mediate GVT effects while limiting GVHD include: (1) allograft T cell depletion followed by immune enhancement; (2) modulation of T cell dose or T cell subset composition; (3) donor lymphocyte infusion; (4) reduced-intens ity host preparation; (5) modulation of Th1/Th2 and Tc1/Tc2 cell balance; (6) cytokine therapy or neutralization ; (7) T regulatory cell therapy; (8) co-stimulatory pathway modulation; (9) chemokine pathway modulation; (10) induction of antigen-specif ic T cells; (11) alloreactive NK cell therapy; and (12) targeted pharmaceutical inhibition of proteosome, mammalian target of rapamycin, and histone deacetylase pathways. Clearly, a multitude of approaches exist that hold promise for separating GVT effects from GVHD. Future success in this endeavor will require a strong commitment towards translational research and continued advances in cell, vaccine, cytokine, monoclonal antibody, and targeted molecular therapy.D Fowler

Source: Critical Reviews in Oncology/Hematology, Vol. 57, No. 3. (March 2006), pp. 225-244.
Host?tumor interactions influencing cancer progression: Drug Discovery Today: Disease Mechanisms, Vol. 2, No. 2. (FebruaryFebru ary 2005), pp. 199-204.Our appreciation of the complexity of tumor biology has led us from considering tumors as autonomous masses of mutant cells to an awareness of the insidious nature of tumors as entities that can hijack and exploit various normal physiologic processes of the host. In this article, we will explore the recent developments in our understanding of how the immune system, extracellular matrix metabolism, interactions with fibroblasts and angiogenesis affect tumor development.B Fingleton, L Coussens

Source: Drug Discovery Today: Disease Mechanisms, Vol. 2, No. 2. (FebruaryFebruary 2005), pp. 199-204.
Plasmodium falciparum multiple infections, disease severity and host characteristic s in malaria affected travellers returning from Africa.: Travel medicine and infectious disease, Vol. 6, No. 4. (July 2008), pp. 205-209.BACKGR OUND: The pathogenesis of malaria is the result of complex interactions between parasites, host and environment. Several studies have assessed the role of genetic characteristic s of Plasmodium falciparum infection in the clinical severity of malaria infection comparing different genotypic determinants in mild and severe cases. The genes encoding the polymorphic merozoite surface proteins 1 (msp-1) and 2 (msp-2) and the dihydrofolate reductase (dhfr) of malaria parasites have been extensively used as markers to investigate the genetic diversity and the population structure of P. falciparum. The aim of this study was to assess the epidemiologica l, clinical, host- and parasite-relat ed determinant factor of the genetic diversity of P. falciparum infections in travellers returning to Italy. METHODS: Between 1998 and 2001, we have retrospectivel y studied 64 inpatients all returning from African malaria-endemi c countries. Designation of severe malaria was determined by using the World Health Organization (WHO) definition. P. falciparum infections detected by species-specif ic PCR were genotyped at the msp-1 and msp-2 loci and clones were determined. PCR and enzyme-digesti on methods were used to screen the mutation occurring at codon 108. RESULTS: Multiple P. falciparum genotypes were detected in 32 patients (50%). The number of genotypes was correlated to different host characteristic s. No association was found between allelic number of msp-1 or msp-2 and season of travel, absence of antimalarial prophylaxis, length of stay or blood parasitemia. At multiple analysis adjusted for few confounding variables, two variables showed a significant association with multiplicity of P. falciparum genotypes: male gender (p=0.018) and severity of disease (p=0.044). CONCLUSION: In our study all but one patients with severe malaria had a infection with a multiplicity of P. falciparum clones. At multivariate analysis the male gender, and the occurrence of severe malaria were significantly more commonly detected in patients affected by imported malaria with multiple clones.E Nicastri, MG Paglia, C Severini, P Ghirga, N Bevilacqua, P Narciso

Source: Travel medicine and infectious disease, Vol. 6, No. 4. (July 2008), pp. 205-209.
Host cell manipulation by the human pathogen Toxoplasma gondii: Cellular and Molecular Life Sciences (CMLS), Vol. 65, No. 12. (19 June 2008), pp. 1900-1915.Abst ract. Toxoplasma gondii is an obligate intracellular parasite that can infect virtually any nucleated cell. During invasion Toxoplasma creates the parasitophorou s vacuole, a subcellular compartment that acts as an interface between the parasite and host, and serves as a platform for modulation of host cell functions that support parasite replication and infection. Spatial reorganization of host organelles and cytoskeleton around the parasitophorou s vacuole are observed following entry, and recent evidence suggests this interior redecorating promotes parasite nutrient acquisition. New findings also reveal that Toxoplasma manipulates host signaling pathways by deploying parasite kinases and a phosphatase, including at least two that infiltrate the host nucleus. Toxoplasma infection additionally controls several cellular pathways to establish an anti-apoptotic environment, and subverts immune cells as a conduit for dissemination. In this review we discuss these recent developments in understanding how Toxoplasma achieves widespread success as a human and animal parasite by manipulating its host.J Laliberté, V Carruthers

Source: Cellular and Molecular Life Sciences (CMLS), Vol. 65, No. 12. (19 June 2008), pp. 1900-1915.
Cancer cell: using inflammation to invade the host: Molecular Cancer, Vol. 6 (16 April 2007), 29.Background Inflammation is increasingly recognized as an important component of tumorigenesis, although the mechanisms involved are not fully characterized. The invasive capacity of cancers is reflected in the classic metastatic cascade: tumor (T), node (N) and metastasis (M). However, this staging system for cancer would also have a tumoral biological significance. Presentation of the hypothesis To integrate the mechanisms that control the inflammatory response in the actual staging system of cancer. It is considered that in both processes of inflammation and cancer, three successive phenotypes are presented that represent the expression of trophic functional systems of increasing metabolic complexity for using oxygen. Testing the hypothesis While a malignant tumor develops it express phenotypes that also share the inflammatory response such as: an ischemic phenotype (anoxic-hypoxi c), a leukocytic phenotype with anaerobic glycolysis and migration, and an angiogenic phenotype with hyperactivity of glycolytic enzymes, tumor proliferation and metastasis, and cachexia of the host. The increasing metabolic complexity of the tumor cell to use oxygen allows for it to be released, migrate and proliferate, thus creating structures of growing complexity. Implication of the hypothesis One aim of cancer gene therapy could be the induction of oxidative phosphorylatio n, the last metabolic step required by inflammation in order to differentiate the tissue that it produces.Jose- Ignacio Arias, Maria-Angeles Aller, Jaime Arias

Source: Molecular Cancer, Vol. 6 (16 April 2007), 29.
Linking within- and between-host dynamics in the evolutionary epidemiology of infectious diseases: Trends in Ecology & Evolution, Vol. 23, No. 9. (September 2008), pp. 511-517.Nested models (also called embedded models) explicitly link dynamical processes that occur at different scales. Recently there has been considerable interest in linking within- and between-host levels of disease dynamics in the study of pathogen evolution. Here we review the extent to which these nested models have increased our understanding of pathogen evolution. We suggest that, although such models have been useful for determining the nature of tradeoffs between epidemiologica l parameters and for evaluating the consequences of conflicting selection pressures at different scales, the vast majority of previous results could likely have been obtained without the use of nested models per se. Nevertheless, these models have proven very useful through their highlighting of the importance of within-host disease dynamics on pathogen evolutionN Mideo, S Alizon, T Day

Source: Trends in Ecology & Evolution, Vol. 23, No. 9. (September 2008), pp. 511-517.
Host Switching in Lyssavirus History from the Chiroptera to the Carnivora Orders: J. Virol., Vol. 75, No. 17. (1 September 2001), pp. 8096-8104.Lyss aviruses are unsegmented RNA viruses causing rabies. Their vectors belong to the Carnivora and Chiroptera orders. We studied 36 carnivoran and 17 chiropteran lyssaviruses representing the main genotypes and variants. We compared their genes encoding the surface glycoprotein, which is responsible for receptor recognition and membrane fusion. The glycoprotein is the main protecting antigen and bears virulence determinants. Point mutation is the main force in lyssavirus evolution, as Sawyer's test and phylogenetic analysis showed no evidence of recombination. Tests of neutrality indicated a neutral model of evolution, also supported by globally high ratios of synonymous substitutions (dS) to nonsynonymous substitutions (dN) (>7). Relative-rate tests suggested similar rates of evolution for all lyssavirus lineages. Therefore, the absence of recombination and similar evolutionary rates make phylogeny-base d conclusions reliable. Phylogenetic reconstruction strongly supported the hypothesis that host switching occurred in the history of lyssaviruses. Indeed, lyssaviruses evolved in chiropters long before the emergence of carnivoran rabies, very likely following spillovers from bats. Using dated isolates, the average rate of evolution was estimated to be roughly 4.3 x 10[-]4 dS/site/year. Consequently, the emergence of carnivoran rabies from chiropteran lyssaviruses was determined to have occurred 888 to 1,459 years ago. Glycoprotein segments accumulating more dN than dS were distinctly detected in carnivoran and chiropteran lyssaviruses. They may have contributed to the adaptation of the virus to the two distinct mammal orders. In carnivoran lyssaviruses they overlapped the main antigenic sites, II and III, whereas in chiropteran lyssaviruses they were located in regions of unknown functions. 10.1128/JVI.75 .17.8096-8104. 2001Hassan Badrane, Noel Tordo

Source: J. Virol., Vol. 75, No. 17. (1 September 2001), pp. 8096-8104.
Antigenic oscillations and shifting immunodominanc e in HIV-1 infections.: Nature, Vol. 375, No. 6532. (15 June 1995), pp. 606-611.A typical protein antigen contains several epitopes that can be recognized by cytotoxic T lymphocytes (CTL), but in a characteristic antiviral immune response in vivo, CTL recognize only a small number of these potential epitopes, sometimes only one, this phenomenon is known as immunodominanc e. Antigenic variation within CTL epitopes has been demonstrated for the human immunodeficien cy virus HIV-1 (ref. 11) and other viruses and such 'antigenic escape' may be responsible for viral persistence. Here we develop a new mathematical model that deals with the interaction between CTL and multiple epitopes of a genetically variable pathogen, and show that the nonlinear competition among CTL responses against different epitopes can explain immunodominanc e. This model suggests that an antigenically homogeneous pathogen population tends to induce a dominant response against a single epitope, whereas a heterogeneous pathogen population can stimulate complicated fluctuating responses against multiple epitopes. Antigenic variation in the immunodominant epitope can shift responses to weaker epitopes and thereby reduce immunological control of the pathogen population. These ideas are consistent with detailed longitudinal studies of CTL responses in HIV-1 infected patients. For vaccine design, the model suggests that the major response should be directed against conserved epitopes even if they are subdominant.MA Nowak, RM May, RE Phillips, S Rowland-Jones, DG Lalloo, S McAdam, P Klenerman, B Köppe, K Sigmund, CR Bangham

Source: Nature, Vol. 375, No. 6532. (15 June 1995), pp. 606-611.
Systems biology and the host response to viral infection: Nature Biotechnology, Vol. 25, No. 12., pp. 1383-1389.Seng -Lai Tan, Gopinath Ganji, Bryan Paeper, Sean Proll, Michael Katze

Source: Nature Biotechnology, Vol. 25, No. 12., pp. 1383-1389.
Host factors exploited by retroviruses: Nature Reviews Microbiology, Vol. 5, No. 4. (26 February 2007), pp. 253-263.Stephe n Goff

Source: Nature Reviews Microbiology, Vol. 5, No. 4. (26 February 2007), pp. 253-263.

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