Sepsis in Special Populations.

Sepsis is recognized by the presence of physiologic and laboratory changes that reflect the inflammatory response to infection on cellular and systemic levels. Comorbid conditions, such as cirrhosis, end-stage renal disease, and obesity, alter patients' susceptibility to infection and their response to it once present. Baseline changes in vital signs and chronic medications often mask clues to the severity of illness.

Differential regulation of the attachment of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected human B cells to extracellular matrix by KSHV-encoded gB and cellular alphaV integrins.

Kaposi's sarcoma-associated herpesvirus (KSHV) has two modes of replications: latent and lytic replications. Reactivation from latency is dictated, in part, by the cell cycle. Herein, we have attempted to delineate the importance of cell cycle in KSHV pathogenesis by exploring the expression pattern of cell-surface receptors during different phases of the cell cycle.

Cigarette smoke concentrate inhibits Kaposi's sarcoma-associated herpesvirus infection.

Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically associated with Kaposi's sarcoma (KS), primary effusion lymphoma(PEL), multicentric Castleman disease, and other tumors. Progression of KS is dictated by an aberrant production of inflammatory cytokines and increase in KSHV infection of cells. In this study, we analyzed the effect of cigarette smoke concentrate (CSC) on KSHV infection of human foreskin fibroblasts (HFF) using real time quantitative RT-PCR.

Spectroscopic analysis of Kaposi's sarcoma-associated herpesvirus infected cells by Raman tweezers.

Kaposi's sarcoma-associated herpesvirus (KSHV), also referred to as human herpesvirus-8 (HHV-8), is a tumor causing virus. KSHV is the cause of several disease conditions known as Kaposi's sarcoma, multicentric Castleman disease, and primary effusion lymphoma. Cell culture supernatants from KSHV infected hematopoietic cells induced angiogenic tubule formation to a significantly greater extent than uninfected hematopoietic cells.

B-Raf-dependent expression of vascular endothelial growth factor-A in Kaposi sarcoma-associated herpesvirus-infected human B cells.

Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV-8) is etiologically linked to Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease. Vascular endothelial growth factor-A (VEGF-A) is one of the essential factors required in KSHV pathogenesis, mainly due to its ability to mediate angiogenesis. In this report we analyzed the relationship between Raf and VEGF-A expression in KSHV-infected hematopoietic cells.

Raf-induced vascular endothelial growth factor augments Kaposi's sarcoma-associated herpesvirus infection.

Recombinant green fluorescent protein encoding Kaposi's sarcoma-associated herpesvirus (rKSHV.152) infection of beta-estradiol stimulated human foreskin fibroblasts (HFF) or HFF/DeltaB-Raf([FF]):ER (expressing a weaker form of B-Raf) could be enhanced to levels comparable to that of HFF/DeltaB-Raf([DD]):ER cells by pretreating cells with soluble vascular endothelial growth factor (VEGF). Conversely, VEGF expression and infection efficiency typically observed in beta-estradiol stimulated HFF/DeltaB-Raf([DD]):ER cells could be lowered significantly by treating with VEGF small interfering RNA.

Role for Raf in the entry of viruses associated with AIDS (review).

The biology of acquired immune deficiency (AIDS) is yet to be completely understood partly because it is complicated by the manifestation of various viral infections and associated pathogenesis. Virus entry into target cells is a key step in the virus replication cycle which is characterized by intricate and complex interactions between virus and host cells. Analyses of virus entry are always hampered to some extent due to the inability to mimic in vivo conditions.

Vascular endothelial growth factor augments human herpesvirus-8 (HHV-8/KSHV) infection.

Human herpesvirus-8 (HHV-8/KSHV) is etiologically associated with Kaposi's sarcoma (KS) and other tumors. The Raf oncoprotein enhances HHV-8 infection of target cells. In addition, we have previously demonstrated that Raf induces vascular endothelial growth factor (VEGF) expression.

Raf promotes human herpesvirus-8 (HHV-8/KSHV) infection.

Human herpesvirus-8 (HHV-8/KSHV) is etiologically associated with Kaposi's sarcoma (KS) and other tumors. Constitutive activation of the mitogen-activated protein kinase (MAPK) signaling pathway has been associated with a variety of tumors, including AIDS-related KS. The oncoprotein Raf is situated at a pivotal position in regulating the MAPK pathway.