DAVID is a popular bioinformatics resource system including a web server and web service for functional annotation and enrichment analyses of gene lists. It consists of a comprehensive knowledgebase and a set of functional analysis tools. Here, we report all updates made in 2021. The DAVID Gene system was rebuilt to gain coverage of more organisms, which increased the taxonomy coverage from 17 399 to 55 464. All existing annotation types have been updated, if available, based on the new DAVID Gene system. Compared with the last version, the number of gene-term records for most annotation types within the updated Knowledgebase have significantly increased. Moreover, we have incorporated new annotations in the Knowledgebase including small molecule-gene interactions from PubChem, drug-gene interactions from DrugBank, tissue expression information from the Human Protein Atlas, disease information from DisGeNET, and pathways from WikiPathways and PathBank. Eight of ten subgroups split from Uniprot Keyword annotation were assigned to specific types. Finally, we added a species parameter for uploading a list of gene symbols to minimize the ambiguity between species, which increases the efficiency of the list upload and eliminates confusion for users. These current updates have significantly expanded the Knowledgebase and enhanced the discovery power of DAVID.

High‐throughput genomics screening studies, such as microarray, proteomics, etc., often result in large, “interesting” gene lists, ranging in size from hundreds to thousands of genes. Given the challenges of functionally interpreting such large gene lists, it is necessary to incorporate bioinformatics tools in the analysis. DAVID is a Web‐based application that provides a high‐throughput and integrative gene functional annotation environment to systematically extract biological themes behind large gene lists. High‐throughput gene functional analysis with DAVID will provide important insights that allow investigators to understand the biological themes within their given genomic study. This unit will describe step‐by‐step procedures to use DAVID tools, as well as a brief rationale and key parameters in the DAVID analysis. Curr. Protoc. Bioinform. 27:13.11.1‐13.11.13. © 2009 by John Wiley & Sons, Inc.

Human papilloma virus (HPV)- IntroductionIt has been demonstrated that both innate and adaptive immune response regulate HIV-1 replication, 1-10 and certain cell types secrete soluble HIV-1-suppressing proteins in response to various stimuli. [11][12][13][14][15] For example, secretion of anti-HIV ␤-chemokines and CD8 antiviral factor (CAF) from human T-lymphotropic virus (HTLV)-type 1 and herpes virus saimiri-infected cell line have been described. [11][12][13][14][15] Although a combination of antibodies and suppressive factors was able to reverse the inhibitory activity of CAF, complete reversal of HIV-1 suppression was not observed, suggesting that additional unknown suppressive factors were involved. 16 Certain microbial organisms elicit immune responses that reduce clinical HIV-1 infection presumably through the induction of soluble suppressive factors. Some persons who are simultaneously infected with HIV-1 and either dengue, Orienta tsutsugamushi, hepatitis G/GB virus C, or measles morbilli virus have reduced viral loads compared with patients who are infected with HIV-1 alone or with HIV-1 and other pathogens. [17][18][19][20][21][22][23][24][25] In the case of hepatitis G virus (HGV), the mechanism of action is postulated to be via binding of the serum HGV E2 protein to CD81, leading to increased regulated on activation normal T expressed and secreted protein (RANTES) secretion and reduced CCR5 expression. 24 In vitro studies have shown that HTLV-type 2 infection might up-regulate the production of macrophage inflammatory protein-1␣ . 26 Recent studies demonstrate that human papillopma virus-like particles (HPV-VLPs) bind to dendritic cells and are able to induce a range of responses in immune cells, notably the expression of anti-HIV-1 cytokines such as interferon-␣ (IFN-␣), interleukin-10 (IL-10), interferon-␥ (IFN-␥), and monocyte chemotactic protein 2 (MCP-2). 27,28 The HPV-VLP vaccine has been demonstrated to be protective against HPV infection. 29-31 HPV-type 16 (HPV16) represents the primary causative agent of cervical cancer. 32 The HPV16 VLPs, composed of the L1 major capsid protein, form nonenveloped icosahedral particles that lack viral DNA but both morphologically and immunologically resemble native virions. 33 Studies suggest that a potent immune response induced by VLPs is through the Toll-like receptor (TLR)/MyD88 pathway in dendritic cells. 27 In the current work, we evaluated the impact of VLPs on HIV-1 replication. Our results demonstrated that VLPs strongly inhibit replication of X4 and R5 HIV-1 in peripheral blood mononuclear cells (PBMCs) and monocyte-derived macrophages (MDMs). It was discovered that the anti-HIV-1 activity of VLPs involved the release of suppressive factors. Gene expression profiles of PBMCs and MDMs demonstrated that VLP treatment up-regulated numerous potential antiviral genes along with the induction of recently described cytokine . Subsequent experiments demonstrated that recombinant IL-27 was able to inhibit X4 and R5 HIV replication. Taken together, these s...