rotating-cell-culture-systems-for-human-cell-culture-human

Rotating Cell Culture Systems for Human Cell Culture: Human Trophoblast Cells as a Model

The field of human trophoblast research aids in  understanding the complex environment established during placentation. Due to the  nature of these ...

A human fibroblast cell line with conditional p53 expression displayed a p53-dependent increase in both the protein and mRNA levels of proliferating cell nuclear antigen (PCNA) after exposure to ionizing radiation (IR). The combination of p53 induction and IR cooperated to activate a transiently expressed human PCNA promoter-reporter gene via a p53-responsive element. Chromatin immunoprecipitation assays with antibodies specific for p53 or p300/CREB-binding protein revealed specific p53-dependent enrichment of PCNA promoter sequences in immunoprecipitates of sheared chromatin prepared from irradiated cells. Maximal and specific association of acetylated histone H4 with the PCNA promoter also depended on p53 induction and exposure to IR. These data demonstrate p53 binding to a target site in the PCNA promoter, recruitment of p300/CREB-binding protein, and localized acetylation of histone H4 in an IR-dependent manner. These molecular events are likely to play a role in mediating activation of PCNA gene expression by p53 during the cellular response to DNA damage. The analyses indicate that the combination of p53 induction and IR activate the PCNA gene via mechanisms similar to that of p21/wild-type p53-activated factor but to a lesser extent. This differential regulation of PCNA and p21/wild-type p53-activated factor may establish the proper ratio of the two proteins to coordinate DNA repair with cell cycle arrest.

Induction of p53-dependent activation of the human proliferating cell nuclear antigen gene in chromatin by ionizing radiation.

Die Induktion der p53-abh&#xE4;ngige Aktivierung des menschlichen proliferierenden cell nuclear antigen-Gens in Chromatin durch ionisierende Strahlung.

The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) promotes tumor progression through activation of matrix metalloproteinase (MMP) activity. MMP-9 is a gelatinase secreted by both cancer cells and surrounding stromal cells, and it contributes to TNF-alpha-stimulated tumor invasion and metastasis. Cyclin-dependent kinase 9 (CDK9), the catalytic component of positive transcription elongation factor-b, phosphorylates serine 2 residues in the C-terminal domain of RNA polymerase II for productive transcription elongation and is up-regulated upon exposure to various stresses. This study investigated roles of CDK9 in TNF-alpha-stimulated MMP-9 expression in human lung adenocarcinoma cells. CDK9 activity was inhibited using three different strategies, including the CDK9 pharmacological inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), a dominant-negative CDK9, and a CDK9-specific small interfering RNA. All three approaches reduced TNF-alpha-mediated accumulation of MMP-9 in the conditioned media as demonstrated by gelatin zymography. In contrast, transforming growth factor-beta1-induced accumulation of MMP-2 was unaffected by DRB. Expression of the MMP-9 gene was examined using reverse transcription real time PCR and using a transient transfection assay to evaluate MMP-9 promoter activity. DRB reduced the TNF-alpha-induced increase in MMP-9 mRNA levels but did not effect transforming growth factor-beta1-induced MMP-2 mRNA expression. Consistently DRB and dominant-negative CDK9 completely abrogated TNF-alpha-stimulated human MMP-9 promoter activity. TNF-alpha did not regulate expression or localization of CDK9 or its regulatory partner Cyclin T. However, TNF-alpha stimulated CDK9 binding to Cyclin T and MMP-9 gene occupancy by both CDK9 and the serine 2-phosphorylated form of RNA polymerase II. Our findings indicate that CDK9 mediates TNF-alpha-induced MMP-9 transcription. Disruption of TNF-alpha signaling using CDK9 inhibitors could serve as a potential therapeutic strategy against tumor invasion and metastasis.

Cyclin-dependent kinase 9 is required for tumor necrosis factor-alpha-stimulated matrix metalloproteinase-9 expression in human lung adenocarcinoma cells.

Cyclin-abh&#xE4;ngige Kinase 9 ist f&#xFC;r den Tumornekrosefaktor-alpha-stimulierte Matrix-Metalloproteinase-9-Expression in menschlichen Lungen-Adenokarzinom-Zellen erforderlich ist.

Human cytomegalovirus (HCMV) is the leading cause of congenital viral infection in the United States and Europe. Despite the significant morbidity associated with prenatal HCMV infection, little is known about how the virus infects the fetus during pregnancy. To date, primary human cytotrophoblasts (CTBs) have been utilized to study placental HCMV infection and replication; however, the minimal mitotic potential of these cells restricts experimentation to a few days, which may be problematic for mechanistic studies of the slow-replicating virus. The aim of this study was to determine whether the human first trimester CTB cell line SGHPL-4 was permissive for HCMV infection and therefore could overcome such limitations. HCMV immediate early (IE) protein expression was detected as early as 3 hours post-infection in SGHPL-4 cells and progressively increased as a function of time. HCMV growth assays revealed the presence of infectious virus in both cell lysates and culture supernatants, indicating that viral replication and the release of progeny virus occurred. Compared to human fibroblasts, viral replication was delayed in CTBs, consistent with previous studies reporting delayed viral kinetics in HCMV-infected primary CTBs. These results indicate that SGHPL-4 cells are fully permissive for the complete HCMV replicative cycle. Our findings suggest that these cells may serve as useful tools for future mechanistic studies of HCMV pathogenesis during early pregnancy.

Permissive human cytomegalovirus infection of a first trimester extravillous cytotrophoblast cell line.

Permissive humane Cytomegalovirus-Infektion eines ersten Trimester extravill&#xF6;sen Zytotrophoblasten Zelllinie.

Latent membrane protein 1 (LMP-1) of Epstein-Barr virus (EBV) promotes tumorigenesis by inhibiting apoptosis. We show that an important antiapoptotic activity of LMP-1 is the inhibition of Bcl2-associated protein X (Bax), a potent proapoptotic protein. BAX expression was regulated by LMP-1 activation of nuclear factor kappaB (NF-kappaB) via the C-terminal activation region 1 (CTAR-1) and CTAR-2. Interestingly, p65/p50 inhibited, whereas p50/p50 increased, BAX promoter activity as demonstrated by overexpression and selective inhibition of these NF-kappaB isoforms. Electrophoretic mobility shift analysis revealed that LMP-1 activates 2 of the 3 NF-kappaB binding sites (kappaB1-kappaB3) in the BAX promoter. LMP-1 induced binding of the NF-kappaB heterodimer p65/p50 to the kappaB2 site and of the p50/p50 homodimer to the kappaB3 site. Promoter mutation analysis revealed that the kappaB2 site is necessary for inhibition of BAX promoter activity and the kappaB3 site, for its activation. However, the activation of the BAX promoter by LMP-1 was observed only in the presence of specific inhibitors of p65/p50. In all other cases, LMP-1 inhibited BAX promoter activity. Most importantly, the antiapoptotic activity of LMP-1 was considerably decreased in cells deficient for BAX. These results indicate that the inhibition of Bax may be an important antiapoptotic activity of LMP-1.

EBV latent membrane protein-1 protects B cells from apoptosis by inhibition of BAX.

EBV latent membrane protein-1 sch&#xFC;tzt B-Zellen durch Apoptose durch Hemmung von BAX.

Recent studies have shown that gamma interferon (IFN-gamma) synergizes with the innate IFNs (IFN-alpha and IFN-beta) to inhibit herpes simplex virus type 1 (HSV-1) replication in vitro. To determine whether this phenomenon is shared by other herpesviruses, we investigated the effects of IFNs on human cytomegalovirus (HCMV) replication.

Synergistic inhibition of human cytomegalovirus replication by interferon-alpha/beta and interferon-gamma.

Synergistische Hemmung der humanen Cytomegalovirus-Replikation durch interferon-alpha/beta und Interferon-gamma.

Nachweis einer HIV-Exposition und vor&#xFC;bergehend in Seroreaktivit&#xE4;t archiviert HIV-negativen Seren schweren Bluter.

Approximately 25% of hemophiliacs that were frequently exposed to blood clotting factor concentrates (CFCs) contaminated with human immunodeficiency virus (HIV) are presently HIV seronegative. In this study, we sought to determine if some of these individuals were at any time transiently HIV seropositive. In the early to mid-1980s the majority of severe hemophilia patients were exposed to CFCs contaminated with HIV. Although many of these hemophiliacs became HIV-positive, a small percentage did not become infected. To determine if some of these individuals successfully resisted viral infection, we attempted to document the presence of transient HIV reactive antibodies in archived plasma samples (1980-1992) from currently HIV-negative severe hemophiliacs who had a high probability of repeated exposure to HIV contaminated CFC. Archived plasma samples were retrospectively tested using an FDA approved HIV-1Ab HIV-1/HIV-2 (rDNA) enzyme immunoassay (EIA) and a HIV-1 Western blot assay (Wb), neither of which were commercially available until the late 1980s, which was after many of these samples had been drawn.

Evidence of HIV exposure and transient seroreactivity in archived HIV-negative severe hemophiliac sera.

Idiopathic pulmonary arterial hypertension (iPAH) is associated with human herpesvirus 8 (HHV8) infection and demonstrates pathological angiogenesis similar to that observed with another HHV8-linked disease, namely Kaposi Sarcoma (KS). Importantly, the HHV8 encoded viral G-protein-coupled receptor (vGPCR) induces KS lesions in a murine model. Investigating the impact of vGPCR expression on the angiogenic activity of human pulmonary arterial endothelial cells (HPAEC) can yield insight into the pathobiology of HHV8-associated vascular disorders, particularly PAH. Cultured HPAECs were transduced with retroviral vectors carrying either control or vGPCR coding regions. vGPCR expression selectively activated matrix metalloproteinase (MMP)-2, a pivotal matrix modulating enzyme during angiogenesis. A membrane type 1 MMP (MT1-MMP) neutralizing antibody and the tissue inhibitor of metalloproteinases-2 (TIMP-2) independently blocked vGPCR-induced MMP-2 activation. vGPCR expression concordantly promoted MMP-2 activation by increasing MT1-MMP expression while decreasing TIMP-2 expression. vGPCR activated Src kinase as demonstrated by phosphorylation of Src and its substrate focal adhesion kinase (FAK). vGPCR promoted angiogenesis of HPAECs as demonstrated by a substantial increase in tubulogenesis in vitro. The Src inhibitors PP2 and SU6656 significantly diminished vGPCR-induced MMP-2 activation and tubulogenesis. Our findings indicate that vGPCR induces MMP-2 activation in HPAECs through regulation of MT1-MMP and TIMP-2 expression. vGPCR activates Src and inhibition of such activation abrogates proMMP-2 activation and in vitro angiogenesis induced by vGCPR. The current study implicates vGPCR as an etiological agent in iPAH and identifies Src and MMP-2 as potential therapeutic targets in HHV8 associated KS and iPAH.

Activation of proMMP-2 and Src by HHV8 vGPCR in human pulmonary arterial endothelial cells.

Idiopathische pulmonale arterielle Hypertonie (iPAH) ist verbunden mit Humanes Herpesvirus 8 (Das HHV-8) Infektion und zeigt pathologische Angiogenesis &auml;hnlich wie mit einer anderen Krankheit das HHV-8-chromosomale, n&auml;mlich Kaposi Sarkom (KS) beobachtet. Wichtig ist, induziert der HHV-8 codierte virale G-Protein-gekoppelter Rezeptor (vGPCR) KS-L&auml;sionen in einem murinen Modell. Untersuchung der Auswirkung von vGPCR Ausdruck auf die Angiogenese-Aktivit&auml;t des menschlichen pulmonale arterielle Endothelzellen kann (HPAEC) einen Einblick in die Pathobiologie das HHV-8-assoziierte vaskul&auml;re Erkrankungen, insbesondere PAH f&uuml;hren. Kultivierten HPAECs wurden mit retrovirale Vektoren, Durchf&uuml;hrung, Kontrolle oder vGPCR Codierung Regionen ausgestrahlt. vGPCR Ausdruck aktiviert selektiv Matrix-Metalloproteasen (MMP)-2, eine zentrale Matrix modulierenden Enzym w&auml;hrend Angiogenesis. Eine Membrane Typ 1 MMP (MT1-MMP) neutralisierende Antik&ouml;rper und die Gewebe-Inhibitor der Metalloproteinasen-2 (TIMP-2) blockiert unabh&auml;ngig vGPCR induziert MMP-2-Aktivierung. vGPCR Ausdruck gef&ouml;rdert &uuml;bereinstimmend MMP-2 Aktivierung durch Erh&ouml;hung MT1-MMP Ausdruck bei gleichzeitiger TIMP-2 Ausdruck. vGPCR aktivierte Src Kinase, wie durch Phosphorylierung des SRK und seine Substrat fokale Adh&auml;sion Kinase (FAK) gezeigt. vGPCR bef&ouml;rdert Angiogenese des HPAECs, wie durch einen deutlichen Anstieg der Tubulogenesis in-vitro gezeigt. Die Src-Inhibitoren PP2 und SU6656 vermindert deutlich vGPCR induziert MMP-2-Aktivierung und Tubulogenesis. Unsere Ergebnisse zeigen, dass vGPCR MMP-2 Aktivierung in HPAECs durch Verordnung MT1-MMP und TIMP-2 Ausdrucks veranlasst. vGPCR aktiviert Src und Hemmung der solche Aktivierung hebt ProMMP-2-Aktivierung und in-vitro Angiogenese von vGCPR induziert. Die aktuelle Studie steht in Verbindung mit vGPCR als &auml;tiologische Agens in iPAH und Src und MMP-2 identifiziert, wie m&ouml;gliche therapeutische Ziele in das HHV-8 KS und iPAH verbunden.

Aktivierung von ProMMP-2 und Src durch das HHV-8 vGPCR im menschlichen pulmonale arterielle Endothelzellen.

Assoziierten Kaposi-Sarkom-Herpesvirus (KSHV) ist die &auml;tiologische Agent von Kaposi-Sarkom (KS), eine h&ouml;chst gef&auml;&szlig;reichen Neubildungen zeichnet sich durch endothelial abgeleitete spindelf&ouml;rmig Tumorzellen. KSHV-infizierten mikrovaskul&auml;re Endothelzellen zeigen erh&ouml;hte Expression von Cyclooxygenase-2-(COX-2) und KS-L&auml;sionen haben hohe Konzentrationen von Prostaglandin E2 (PGE2), eine kurzlebige Eikosanoide abh&auml;ngig von Cyclooxygenase-Aktivit&auml;t, die mit der Pathogenese der anderen Neoplasias verkn&uuml;pft ist. Um festzustellen, ob die erh&ouml;hte COX-2-Expression und PGE2 Produktion wird vermittelt durch die Angiogenese und tumorigenic KSHV-codierte G-Protein-gekoppelter Rezeptor (vGPCR), entwickelten wir eine rekombinante Retroviren, schnelles vGPCR im menschlichen Nabelschnur Vascular Endothelial Zellen (HUVEC).

Kaposi-Sarkom assoziiert Herpesvirus G-Protein-gekoppelte Rezeptoren Aktivierung der Cyclooxygenase-2 in den vaskul&auml;ren endothelialen Zellen.

Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin E2 (PGE2), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and PGE2 production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC).

Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells.

The role of the pro-inflammatory peptide, LL-37, and its pro-form, human cationic antimicrobial protein 18 (hCAP-18), in cancer development and progression is poorly understood. In damaged and inflamed tissue, LL-37 functions as a chemoattractant, mitogen and pro-angiogenic factor suggesting that the peptide may potentiate tumor progression. The aim of this study was to characterize the distribution of hCAP-18/LL-37 in normal and cancerous ovarian tissue and to examine the effects of LL-37 on ovarian cancer cells. Expression of hCAP-18/LL-37 was localized to immune and granulosa cells of normal ovarian tissue. By contrast, ovarian tumors displayed significantly higher levels of hCAP-18/LL-37 where expression was observed in tumor and stromal cells. Protein expression was statistically compared to the degree of immune cell infiltration and microvessel density in epithelial-derived ovarian tumors and a significant correlation was observed for both. It was demonstrated that ovarian tumor tissue lysates and ovarian cancer cell lines express hCAP-18/LL-37. Treatment of ovarian cancer cell lines with recombinant LL-37 stimulated proliferation, chemotaxis, invasion and matrix metalloproteinase expression. These data demonstrate for the first time that hCAP-18/LL-37 is significantly overexpressed in ovarian tumors and suggest LL-37 may contribute to ovarian tumorigenesis through direct stimulation of tumor cells, initiation of angiogenesis and recruitment of immune cells. These data provide further evidence of the existing relationship between pro-inflammatory molecules and ovarian cancer progression.

Ovarian cancers overexpress the antimicrobial protein hCAP-18 and its derivative LL-37 increases ovarian cancer cell proliferation and invasion.

Die Rolle des Pro-inflammatorische Peptid, LL-37 und sein pro-form, menschliche kationische antimikrobielle Protein 18 (hCAP-18), in Krebs-Entstehung und Progression ist oft missverstanden. Besch&auml;digte und entz&uuml;ndeten Gewebe fungiert LL-37 als Botenstoffe, Mitogen und Pro-angiogenen Faktor darauf hindeutet, dass das Peptid Tumor Fortschreiten potenzieren kann. Ziel dieser Studie war die Verteilung der hCAP-18/LL-37 in normalen und krebsartigen ovariellen Gewebe zu charakterisieren und die Auswirkungen der LL-37 auf Eierstockkrebs Zellen pr&uuml;fen. Ausdruck der hCAP-18/LL-37 wurde auf immun- und Granulosa Zellen von normalen ovariellen Gewebe lokalisiert. Eierstockkrebs wird hingegen deutlich h&ouml;here Ebenen der hCAP-18/LL-37 wo Ausdruck beobachtet wurde im Tumor und stromal Zellen angezeigt. Proteinexpression wurde statistisch im Vergleich zu den Grad der Immunzellen Infiltration und Microvessel Dichte in epithelialen abgeleitete Eierstockkrebs und eine signifikante Korrelation wurde f&uuml;r beide beobachtet. Es wurde gezeigt, dass Eierstock Tumor Gewebe Lysates und Eierstock-Krebs-Zelllinien hCAP-18/LL-37 Ausdr&uuml;cken. Behandlung von Eierstockkrebs Zelllinien mit rekombinantem LL-37 stimuliert Vermehrung, Chemotaxis, Invasion und Matrix-Metalloproteasen Ausdruck. Diese Daten demonstrieren erstmals die hCAP-18/LL-37 ist deutlich in ovariellen Tumoren &uuml;berexprimiert und empfehle LL-37 zu Eierstock-Tumorentstehung durch direkte Stimulation von Tumorzellen, Einleitung der Angiogenese und Rekrutierung von Immunzellen beitragen kann. Diese Daten liefern weitere Beweise f&uuml;r die vorhandene Beziehung zwischen Pro-inflammatorische Molek&uuml;le und Eierstockkrebs Fortschreiten.

Eierstockkrebs &uuml;berexprimiert die antimikrobielle Protein hCAP-18 und erh&ouml;ht seine Derivative LL-37, ovarian Krebs Zellproliferation und Invasion.

Trophoblast invasion is a temporally and spatially regulated scheme of events that can dictate pregnancy outcome. Evidence suggests that the potent mitogen epidermal growth factor (EGF) regulates cytotrophoblast (CTB) differentiation and invasion during early pregnancy.

Epidermal growth factor-stimulated extravillous cytotrophoblast motility is mediated by the activation of PI3-K, Akt and both p38 and p42/44 mitogen-activated protein kinases.

Trophoblast Invasion ist ein zeitlich und r&auml;umlich geregelten System von Ereignissen, die Schwangerschaft diktieren k&ouml;nnen. Anhaltspunkte daf&uuml;r, dass der potente Mitogen-epidermalen Wachstumsfaktor (EGF) Cytotrophoblast (CTB) Differenzierung und Invasion w&auml;hrend der fr&uuml;hen Schwangerschaft regelt.

Epidermaler Wachstumsfaktor stimuliert extravillous Cytotrophoblast Motilit&auml;t ist durch die Aktivierung der PI3-K, Akt und p38 und p42/44 Mitogen-aktivierte Proteinkinasen vermittelt.

Human cytomegalovirus (HCMV) is the most prevalent congenital viral infection in the United States and Europe causing significant morbidity and mortality to both mother and child. HCMV is also an opportunistic pathogen in immunocompromised individuals, including human immunodeficiency virus (HIV)- infected patients with AIDS, and solid organ and allogeneic stem cell transplantation recipients. Current treatments for HCMV-associated diseases are insufficient due to the emergence of drug-induced resistance and cytotoxicity, necessitating novel approaches to limit HCMV infection. The aim of this study was to develop therapeutic peptides targeting glycoprotein B (gB), a major glycoprotein of HCMV that is highly conserved across the Herpesviridae family, that specifically inhibit fusion of the viral envelope with the host cell membrane preventing HCMV entry and infection.

Peptide inhibition of human cytomegalovirus infection.

Menschliche Cytomegalievirus (HCMV) ist die am weitesten verbreitete angeborene Virusinfektion in den Vereinigten Staaten und Europa, die signifikante Morbidit&auml;t und Mortalit&auml;t f&uuml;r Mutter und Kind verursachen. HCMV ist auch eine opportunistische Erreger bei immungeschw&auml;chten Personen, einschlie&szlig;lich Human Immunodeficiency Virus (HIV)-infizierten Patienten mit AIDS, und solide Orgel und allogene Stammzell-Transplantation-Empf&auml;nger. Aktuelle Behandlungen f&uuml;r HCMV-assoziierten Krankheiten sind unzureichend, aufgrund des Entstehens von Arzneimittel-induzierter Widerstand und Zytotoxizit&auml;t, erfordern neue Ans&auml;tze um HCMV Infektion zu begrenzen. Ziel dieser Studie war therapeutische Peptide Glykoprotein B (gB), einem gro&szlig;en Glykoprotein von HCMV, die stark in der Familie der Herpesviridae konserviert ist gezielt zu entwickeln, die speziell Verschmelzung der viralen H&uuml;lle mit der Zellmembran Host HCMV-Eintrag und Infektion verhindern hemmen.

Article	Year
Induction of p53-dependent activation of the human proliferating cell nuclear antigen gene in chromatin by ionizing radiation. The Journal of biological chemistry\| PubMed ID: 12947108	2003
Cyclin-dependent kinase 9 is required for tumor necrosis factor-alpha-stimulated matrix metalloproteinase-9 expression in human lung adenocarcinoma cells. The Journal of biological chemistry\| PubMed ID: 15528190	2005
Permissive human cytomegalovirus infection of a first trimester extravillous cytotrophoblast cell line. Virology journal\| PubMed ID: 15548334	2004
EBV latent membrane protein-1 protects B cells from apoptosis by inhibition of BAX. Blood\| PubMed ID: 15613549	2005
Synergistic inhibition of human cytomegalovirus replication by interferon-alpha/beta and interferon-gamma. Virology journal\| PubMed ID: 15727684	2005
Evidence of HIV exposure and transient seroreactivity in archived HIV-negative severe hemophiliac sera. Virology journal\| PubMed ID: 16107217	2005
Activation of proMMP-2 and Src by HHV8 vGPCR in human pulmonary arterial endothelial cells. Journal of molecular and cellular cardiology\| PubMed ID: 17188706	2007
Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells. Virology journal\| PubMed ID: 17868457	2007
Ovarian cancers overexpress the antimicrobial protein hCAP-18 and its derivative LL-37 increases ovarian cancer cell proliferation and invasion. International journal of cancer. Journal international du cancer\| PubMed ID: 17960624	2008
Epidermal growth factor-stimulated extravillous cytotrophoblast motility is mediated by the activation of PI3-K, Akt and both p38 and p42/44 mitogen-activated protein kinases. Human reproduction (Oxford, England)\| PubMed ID: 18487214	2008
Peptide inhibition of human cytomegalovirus infection. Virology journal\| PubMed ID: 21342525	2011

Cindy A. Morris

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