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Herpes simplex virus (HSV) is common throughout the world and is a target for vaccine development. Transcutaneous immunisation is a novel technique that uses the application of vaccine antigens in solution on the skin in the presence of cholera toxin (CT) as an adjuvant. This study investigated the potential of transcutaneous immunisation in C3H mice, using CT co-administered with whole inactivated HSV-1 (CT+HSVi) or HSV-1 antigens extracted from infected Vero cells (CT+HSVag) or a control protein (CT+BSA). The application of any of the three vaccines on to bare mouse skin resulted in the migration of Langerhans cells from the epidermis and in the production of serum antibodies to CT. Both HSV preparations generated serum and mucosal (faecal) antibodies to HSV, with the CT+HSVi vaccine being a more potent stimulator of humoral immunity. The CT+HSVag vaccine, however, was the more potent stimulator of cell-mediated immunity, giving rise to a strong delayed type hypersensitivity response and lymphocyte proliferation in vitro. When the mice were challenged by epidermal inoculation of HSV, the CT+HSVag vaccine induced a higher level of protection than the CT+HSVi vaccine, a result which may indicate that the efficacy of HSV vaccines depends on stimulation of cell-mediated rather than humoral responses. The success of topical vaccination suggests that the transcutaneous route may offer a promising potential for novel vaccine delivery which merits further investigation.

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Ultraviolet B (UV-B) irradiation suppresses cell-mediated immunity and may lead to increased susceptibility to infectious diseases. Limited evidence suggests that exposure promotes a T helper (Th) 2 type of cytokine response with abrogation of a Th1 response. Several putative mediators of UV-induced immunosuppression have been identified, of which interleukin-4 (IL-4), an example of a Th2 cytokine, is one. Primary and secondary epidermal infections with herpes simplex virus (HSV) type 1 in IL-4 knockout (IL-4-/-) mice and the parent strain Bb 129 strain (IL-4+/+) were investigated using clinical features, phenotyping of cells from lymph nodes draining the sites of infection and lymphoproliferation assays. The IL-4-/- mice were more susceptible to both primary and secondary HSV infections than the parent mice. The percentage of lymph node dendritic cells (DC) expressing Ia was 45 in the IL-4+/+ mice but only 18 in the IL-4-/- strain, and the lymph node cells from infected IL-4-/- mice were less able to respond in vitro to HSV than those from the parent strain. Following suberythemal UV-B irradiation, more severe primary and secondary lesions resulted in both strains. There were fewer lymph node DC expressing Ia in both strains and this change was accompanied by suppression of the lymphoproliferation induced by HSV which was due to an effect on DC function rather than on the proliferative ability of the responding lymphocytes. UV-B exposure had no effect on ICAM-1 or B7.2 expression on the DC. Thus IL-4 seems to protect mice against HSV infection, and no evidence was obtained for the involvement of IL-4 in the UV-induced immunomodulation which results in more severe cutaneous HSV infections.

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Solar radiation contains ultraviolet B (280-315 nm) and ultraviolet A (ultraviolet AII, 315-340 nm; ultraviolet AI, 340-400 nm) wavebands. Ultraviolet B is known to suppress certain aspects of cell mediated immunity. Using three ultraviolet lamps (the broad-band ultraviolet B TL-12, the narrow-band ultraviolet B TL-01 and an ultraviolet AI source), we investigated the dose and waveband dependencies for the suppression of contact hypersensitivity to oxazolone and delayed-type hypersensitivity to herpes simplex virus, plus the formation of cis-urocanic acid in C3H/HeN mice. A single exposure of 1500 J/m2 TL-12 or 10,000 J/m2 TL-01 or 500,000 J/m2 ultraviolet AI corresponded to 1 minimum erythema dose in this mouse strain. The percentage of cis-urocanic acid of the total urocanic acid rose from a background level of 1.7% to 40% with 1000 J/m2 TL-12 or 10,000 J/m2 TL-01, but only 17% cis-urocanic acid was obtained with 500,000 J/m2 ultraviolet AI. The contact hypersensitivity response was significantly suppressed after a minimum dose of 5000 J/m2 TL-12 or 50,000 J/m2 TL-01 or 500,000 J/m2 ultraviolet AI. The delayed-type hypersensitivity response was suppressed by a minimum dose of 100 J/m2 TL-12 or 10,000 J/m2 TL-01 or 1000 J/m2 ultraviolet AI. So, whereas a low dose of ultraviolet AI reduced the delayed-type hypersensitivity response, a 500-fold higher dose was required to suppress contact hypersensitivity. There was no correlation between the suppression of these responses and the concentration of cis-urocanic acid in the skin. Thus different mediators may modulate the various immune responses affected by ultraviolet exposure, depending on the wavelength of the radiation.

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Exposure to UV is a recognised risk factor for skin cancer and it also induces immunosuppression to a variety of antigens encountered following the irradiation. The latter property has been demonstrated in rodent models of infections with the microbial agents including viruses, bacteria, protozoa and helminths. In the majority of cases the severity of the symptoms and the microbial load in the host are increased as a result of the immunomodulation. UV can also affect the pathogenesis of some natural microbial infections of human subjects, such as causing recrudescence of herpes simplex virus and contributing to the oncogenic potential of papillomaviruses. Sufficient data have been generated from the animal models to construct a risk assessment in humans for suppression of microbial immune responses induced by sunlight exposure. This estimation requires verification from epidemiological studies and from further work to assay modulation in human immunity to particular pathogens experienced before and after the UV radiation.

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Ultraviolet B (UVB) exposure suppresses cell-mediated immunity and may alter the cytokine profile, reducing T helper 1 (Th1) cytokines and promoting Th2 cytokines. Th1 cytokines enhance the production of immunoglobulin (Ig) G2a, IgG2b and IgG3 antibodies, while Th2 cytokines enhance the production of IgG1 and IgE antibodies. The effect of suberythemal UVB irradiation on antibody isotypes following infection of C3H/HeN mice with herpes simplex virus (HSV) was investigated using two protocols. First, mice were irradiated prior to two subcutaneous infections with HSV. Second, mice were immunised with inactivated HSV before being irradiated and challenged epidermally with HSV, which led to an increase in the size of the clinical lesions compared with unirradiated animals. In both models, the HSV-specific IgG titre was not affected by the UVB exposure but, generally, the irradiated animals showed a small reduction in both Th1- and Th2-associated HSV antibody isotypes. IL-4 knockout (IL-4-/-) mice were used to investigate the role of IL-4 in UVB-induced isotype switching. Here IL-4-/- and IL-4+/+ strains were irradiated prior to primary and secondary epidermal infections with HSV, followed by measurement of antibody titres and lesion size. In both the mutant and parent mice, UV irradiation led to an increase in lesion severity. In IL-4+/+ mice, UV exposure did not affect the HSV titre of any of the individual isotypes tested but did suppress the total IgG to HSV This suppression may be due to UV-induced IL-4 release because, in the IL-4-/- mice, HSV IgG was elevated by the UVB irradiation. If UV modulates the immune response solely via the action of cytokines, then the downregulation of Th1 cytokines and upregulation of Th2 cytokines should be accompanied by antibody isotype switching from IgG2a and IgG3 towards IgG1 and IgE. This result was not obtained in the models tested, perhaps because HSV infection promotes such a complex array of innate and acquired immune responses that a clear effect on virus-specific isotype production may not be apparent.

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Prolonged exposure to ultraviolet light (UV) is known to lead to premature skin ageing, increased incidence of cataract and a high risk of developing skin cancers. UV-B irradiation, even if given as a single suberythemal dose, suppresses some immune responses, possibly reducing the production of T helper (Th) 1 cytokines [interleukin (IL)-2 and interferon-gamma] and augmenting Th2 cytokines (IL-4, IL-5 and IL-10) in mice. We investigated the role of IL-4 in UV-B induced immunomodulation using IL-4 knockout (IL-4 -/-) mice and the parent strain Bb129. Suberythemal UV-B irradiation (1440 J/m2) led to a reduction in the density and antigen presenting ability of Langerhans' cells in the epidermis of both normal and IL-4 -/- mice. Exposure also induced an accumulation of CD4+ and CD8+ lymphocytes as well as dendritic cells in the lymph nodes draining the irradiated site in both strains. The proliferation of lymph node cells in response to the mitogen concanavalin A was enhanced in the IL-4 -/- mice compared with the parent strain. Following UV-B exposure, this proliferation was increased in lymph node cells of parent mice but was significantly suppressed in the IL-4 -/- mice. The contact hypersensitivity (CH) response to oxazolone was suppressed to the same extent by UV-B irradiation in both strains. In the parent mice, infected with herpes simplex virus (HSV) following UV-B exposure and challenged subsequently with inactivated virus, the delayed hypersensitivity (DH) response was suppressed by about 50% compared with unirradiated mice; no such suppression in DH occurred in irradiated IL-4 -/- mice infected with HSV. Thus, IL-4 may be an important mediator of the UV-B-induced suppression in DH but not in CH, where other cytokines may be involved or may compensate for the lack of IL-4.

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Studies in experimental models have implicated histamine and prostanoids in ultra-violet B (UVB)- and cis-urocanic acid (UCA)-induced systemic immunosuppression. This study examined the hypothesis that UVB irradiation and cis-UCA suppressed contact hypersensitivity responses to hapten by induction of histamine, which in turn evoked a prostanoid-dependent component of immunosuppression. BALB/c mice were administered with a cis-UCA monoclonal antibody, a combination of histamine types 1 and 2 receptor antagonists, or indomethacin. Mice were sensitized to 2,4,6-trinitrochlorobenzene (TNCB) on their ventral surface 5 days after UVB irradiation, or cis-UCA or histamine administration. Ears were challenged with TNCB 5 days later. Cis-UCA antibody inhibited the suppressive effects of UVB by approximately 60% and confirmed that suppression of contact hypersensitivity responses by UVB was due, at least in part, to mechanisms involving cis-UCA. Histamine suppressed contact hypersensitivity responses and the effects of cis-UCA and histamine were not cumulative, suggesting that cis-UCA and histamine signal largely through the same pathway. The immunosuppressive effects of histamine were not affected by the cis-UCA antibody, consistent with the model that histamine acts downstream of cis-UCA. Administration of histamine receptor antagonists and indomethacin each approximately halved the UVB- and cis-UCA-induced systemic suppression of contact hypersensitivity responses. The effects of the reagents that inhibited the action of histamine and prevented prostanoid production were not cumulative, and suggested involvement in the same pathway. These results support the involvement of cis-UCA, histamine and prostanoids, in a sequence, in UVB-induced systemic suppression of contact hypersensitivity responses.

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Trans-urocanic acid (trans-UCA) accumulates in the upper layers of the epidermis and can be isomerized to cis-UCA by UV light irradiation. Cis-urocanic acid possesses immunosuppressive properties that have led to its consideration as one of the initiators of UV-induced immunosuppression. High quantities of cis-UCA persist in human skin for prolonged periods in the summer months. In the present study, mice were injected intradermally with trans-UCA and cis-UCA three times a week for 4 weeks in order to ascertain the long-term effects of the presence of these compounds in the skin. The weight of mice and of their spleens were unaffected by the cis- or trans-UCA treatment. A decrease in thymus weight, accompanied by an increase in lymph node weight, was detected in the cis-UCA-treated mice compared with trans-UCA-treated mice and untreated controls. A net accumulation of lymphocytes and dendritic cells (DC) in lymph nodes was evident following cis-UCA treatment but the percentage of both CD4+ and CD8+ lymphocytes as well as Ia+ DC remained constant among the different treatment groups, indicating that there was no specific migration or proliferation of a particular subset of cells. The in vitro lymphoproliferative response of lymph node cells to the mitogen concanavalin A was significantly sup pressed by cis-UCA treatment. The density of Langerhans cells in the epidermis of the ears was not altered by the chronic cis-UCA treatment. However, chronic cis-UCA treatment did suppress the mixed skin lymphocyte reaction response utilizing epidermal cells from the ears (an uninjected area of skin), indicating a systemic suppression. Compared with trans-UCA treatment, chronic cis-UCA treatment did not cause a significant reduction in the contact hypersensitivity response to oxazolone or the delayed hypersensitivity response to herpes simplex virus. Thus, chronic treatment with cis-UCA led to the suppression of some, but not all, of the immune parameters that are affected by UVB irradiation.

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The narrow-band UVB (TL01) lamp (311 nm emission) was developed for use in phototherapy, as an alternative to a broad-band UVB source and to photochemotherapy, both of which have significant side effects and carry a risk of carcinogenesis. This new lamp has proved to be particularly effective at clearing psoriasis. It is now acknowledged that the TL01 lamp is probably 2-3 times more carcinogenic per minimum erythema dose than broad-band UVB, but the cumulative dose required in therapy is considerably less than when using broad-band UVB sources. In terms of irradiation dose, the TL01 lamp is about 5-10-fold less potent than broad-band UVB for erythema induction, hyperplasia, oedema, sunburn cell formation and Langerhans cell depletion from skin. However, the broad-band UVB to TL01 potency ratio for cis-urocanic acid formation in the skin is approximately unity. In addition, the TL01 lamp, as used in phototherapy, has relatively more suppressive effects than broad-band UVB on systemic immune responses as judged by natural killer cell activity, lymphoproliferation and cytokine responses. However, the TL01 lamp is less effective at reducing epidermal antigen presentation, inducing dendritic cell migration to lymph nodes draining irradiated sites and suppressing contact hypersensitivity at the doses tested. Therefore the use of the TL01 lamp in phototherapy should be considered carefully after weighing up its diverse effects on the skin and immune system.

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Exposure to ultraviolet B (UVB) radiation results in the suppression of many cell-mediated immune responses, and recent studies mice and murine cells in vitro suggest a shift from a T-helper 1 (Th1) to a Th2 type of response on irradiation. Active psoriasis is considered to be a Th1-type disorder, chiefly on the basis of the cytokines produced by inflammatory cells in psoriatic lesions. We investigated the effect of phototherapy in patients with psoriasis on the cytokine profile of mitogen-stimulated mononuclear cells from peripheral blood and the concentration of IgG subclasses and IgE in the plasma. Eight patients were irradiated with a broad-band UV source (Sylvania UV6; 280-400 nm) three times a week and another eight with a narrow-band UVB source (Philips TL-01; 311-313 nm). Peripheral blood was collected before therapy started and after 1-4 weeks of therapy. Peripheral blood mononuclear cells were stimulated in vitro with phytohemagglutinin; proliferation was measured by incorporation of tritiated thymidine and culture supernatants assayed for interleukin (IL)-2, -4 and -10 and gamma-interferon (IFN) by enzyme-linked immunosorbent assays. Lymphoproliferation was not consistently affected by 4 weeks of UV6 therapy, and there was also no consistent change in the production of IL-2, IL-10 or gamma-IFN. In contrast, 4 weeks of TL-01 therapy significantly suppressed lymphoproliferative responses. In addition the production of IL-2, IL-10 and gamma-IFN was lowered after 1 week of TL-01 therapy, and this was even more apparent after the treatment had been extended to 4 weeks. IL-4 concentrations were below detectable levels in all the samples throughout the study. The amounts of IgG1, -2, -3 and -4 and IgE in the plasma of the patients did not vary with either of the two phototherapies. Thus, although no evidence was obtained to indicate that UV6 exposures affected T-helper subsets in psoriasis, TL-01 inhibited the activity of both Th1 and Th2 subsets while not altering plasma antibody concentrations.

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Orolabial human infections with herpes simplex virus type 1 (HSV-1) are very common; following the primary epidermal infection, the virus is retained in a latent form in the trigeminal ganglia from where it can reactivate and cause a recrudescent lesion. Recrudescences are triggered by various stimuli including exposure to sunlight. In this review three categories of mouse models are used to examine the effects of UV irradiation on HSV infections: these are UV exposure prior to primary infection, UV exposure as a triggering event for recrudescence and UV exposure prior to challenge with virus in mice already immunized to HSV. In each of these models immunosuppression occurs, which is manifest, in some instances, in increased morbidity or an increased rate of recrudescence. Where known, the immunological mechanisms involved in the models are summarized and their relevance to human infections considered.

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Previous studies have indicated that suberythemal ultraviolet B (UV-B) irradiation of C3H mice before primary infection with herpes simplex virus (HSV) type 1 does not result in increased morbidity or mortality, but a suppressed delayed type hypersensitivity (DH) to the virus can be demonstrated. Any effect of UV radiation on pathogenesis during secondary epidermal HSV infection has not been previously examined. Mice were immunized by subcutaneous injection of inactivated HSV and, 5 days later, one group was UV-B-irradiated. The next day all mice were challenged epidermally with HSV. Most of the mice (92%) in the irradiated group developed severe lesions, whilst 59% of the non-irradiated group had mild lesions and 30% no lesions. Infectious virus was not isolated from the adrenal glands after challenge in either group. In addition, the DH to the virus was not affected by the UV exposure. The numbers of lymphocytes and dendritic cells in the lymph nodes draining the site of epidermal infection were increased in the UV group compared with the non-irradiated group. Following challenge, the percentage of CD4+ and CD8+ lymphocytes in lymph nodes was unaltered but the MHC class II expression on dendritic cells in these lymph nodes was reduced by UV exposure. The lymphoproliferative response in vitro of lymph node cells revealed a suppressed response to HSV and to the mitogen concanavalin A in the irradiated group. Thus, UV irradiation prior to epidermal secondary infection with HSV led to more severe infections due, perhaps, to a modulation in local antigen presentation.

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C3H mice were irradiated three times a week for up to 6 weeks with either 500 J/m2 or 1000 J/m2 broadband UVB (270-350 nm) or 3000 J/m2 narrowband UVB (311-312 nm; TL01 source). Each dose was suberythemal to the mouse strain used. The number of Langerhans cells (LC) in the epidermis was reduced by over 50% after 2 weeks of irradiation with the UVB source and by 20% following TL01 irradiation. Continued irradiation for up to 6 weeks resulted in no further decrease in LC numbers in the case of the UVB source but a steady decline to 40% in the case of the TL01 source. Sunburn cells were detected following irradiation with both sources but the numbers were very low in comparison with acute exposure. Ultraviolet-B exposure resulted in doubling of the thickness of the epidermis throughout the 6 weeks of irradiation while TL01 exposure did not alter epidermal thickness. Conversion of trans- to cis-urocanic acid (UCA) was observed with both UVB and TL01 sources. The percentage of cis-UCA started to return to normal after 4 weeks of TL01 exposure despite continued irradiation. As observed following a single exposure, the contact hypersensitivity (CH) response was significantly reduced following 6 weeks of UVB irradiation but was unaffected by TL01 exposure, indicating no correlation between cis-UCA levels and CH response. Total serum immunoglobulin levels remained unchanged throughout the 6 weeks of UVB or TL01 irradiation but IgE titers significantly increased in all cases in the first 2 weeks of irradiation, indicating a possible shift to a TH2 cytokine profile.(ABSTRACT TRUNCATED AT 250 WORDS)

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Ultraviolet B (UVB) irradiation of C3H mice causes suppression of delayed hypersensitivity and contact hypersensitivity (CH) to antigens encountered following exposure, and is accompanied by a reduction in Langerhans cell (LC) numbers in the epidermis, loss of epidermal antigen-presenting cell function, and accumulation of dendritic cells in lymph nodes draining the site of irradiation. Various photoreceptors and mediators of these changes have been proposed, one of which is cis-urocanic acid (cis-UCA) formed from the naturally occurring trans-UCA in the epidermis on UV irradiation. A monoclonal antibody that reacts with cis-UCA has become available recently and has been used in this study to clarify the role of UCA. Pretreatment of C3H mice with the monoclonal antibody abrogated the UVB-induced and cis-UCA-induced reduction in epidermal LC numbers. It also prevented the UV-induced suppression of epidermal antigen-presenting cell ability as measured by the mixed skin lymphocyte response. However, it had no effect on the accumulation of dendritic cells in lymph nodes draining the site of UV exposure. With regard to hypersensitivity responses, it did not prevent UV-induced suppression of CH to oxazolone at a range of concentrations but it restored to normal the UV-suppressed delayed hypersensitivity to herpes simplex virus, if administered before exposure. Thus cis-UCA is involved in some UV-induced changes in murine skin but not in others, where alternative mediators, such as tumor necrosis factor-alpha, may be more important.

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Although broadband UV-B irradiation has been shown to induce selective immunosuppression in a variety of experimental systems, the wavelength dependence of the immunomodulation and the initial events in the skin remain unclear. In the present study three UV lamps were used at suberythermal doses on C3H mice: a conventional broadband UV-B source (270-350 nm), a narrowband UV-B source (311-312 nm) and a UV-A source (320-400 nm). Their effects on the photoisomerization of the naturally occurring trans-isomer of urocanic acid (UCA) to cis-UCA, on the density of Langerhans cells and on the ability of epidermal cells to stimulate allogeneic lymphocytes in the mixed skin lymphocyte reaction (MSLR) were ascertained. Broadband UV-B irradiation was more efficient than narrowband UV-B at reducing the density and function of Langerhans cells, while UV-A irradiation was least effective. These changes were most pronounced immediately following irradiation, were dose dependent and were only detected in UV-exposed areas of skin. There was a close correlation between the UV-induced reduction in Langerhans cell density and the formation of cis-UCA in the epidermis. This correlation was not detected between the reduction in the MSLR response following UV irradiation in vivo and cis-UCA formation.

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The coding assignments of the medium-sized (M) RNA segment of the Dugbe (DUG) virus (Nairovirus, Bunyaviridae) were investigated. The complete nucleotide sequence of 4888 nucleotides (nt) contained one long open reading frame in the viral complementary RNA, extending from an AUG start codon at nt 48-50 to a stop codon at nt 4701-4703 (numbered from the 5' terminus of vcRNA). Comparison of the terminal sequences with the ends of the DUG S segment revealed sequence identity between the first nine nucleotides of both segments. No sequence homologies were found with the M segments of other members of the Bunyaviridae, or with their polypeptide products. Expression of portions of the DUG M open reading frame in Escherichia coli demonstrated the carboxyl terminal region of the M open reading frame codes for the G1 structural glycoprotein, which is the target for neutralising antibodies. Confirmation of this assignment was obtained by sequencing the amino terminus of the G1 protein. Two nonstructural glycoproteins which share epitopes with G1 were identified in virus-infected cells, one of which (85 kDa) is processed over a period of several hours to produce G1. The G2 coding region was located upstream of the G1 sequence. The region between the carboxyl terminus of G2 and the 5' end of the long open reading frame apparently encodes a nonstructural protein of about 70 kDa, which is a precursor of the G2 protein.

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The reovirus receptor on mammalian cells has not been fully characterized and controversy exists over the nature of this receptor. We report here that the expression of this receptor is dependent on the differentiation status of a human promyelocytic leukaemia cell line (HL60). Phorbol treatment of HL60 cells for 24 h, at a concentration range of 160 nM down to 1 nM, led to differentiation of these cells towards monocytes and a loss of approximately 80% of their ability to bind reovirus in a fluorescence assay. These cells also lost their susceptibility to T1 and T3 reovirus infection. DMSO treatment for 24 h at a concentration of 1.25% (v/v) led to differentiation towards granulocytes. This was accompanied by an increase of approximately 15% in binding of reovirus to these cells. After being infected by T1 or T3 reovirus, the granulocytes produced higher titres of progeny virus than did untreated HL60 cells. Similar differences were noted when virus binding to HL60 cells was assayed using radiolabelled reovirus. These effects were not detected when murine L fibroblasts were treated with DMSO or phorbol. ATCC-derived murine R1.1 cells did not bind reovirus. Competition data indicated that there may be two reovirus receptors on HL60 cells, and that T1 can bind to only one receptor whereas T3 can bind to both receptors. Our data also suggested that the beta-adrenergic receptor was unlikely to act as the reovirus receptor on HL60 cells.

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The small (S) RNA segment of Dugbe (DUG) virus (Nairovirus, Bunyaviridae) encodes a single protein, the nucleocapsid (N) protein, of M(r) 49.4 kDa. cDNA derived from the complete coding region for the N protein was cloned into Autographa californica nuclear polyhedrosis virus (AcNPV) under control of the polyhedrin promoter and used to infect Spodoptera frugiperda insect cells. Western blotting analysis using monoclonal antibodies demonstrated the production of DUG N protein in the infected cells. Monoclonal and polyclonal antibodies to the N protein of Crimean-Congo haemorrhagic fever (CCHF) virus were found to cross-react weakly with the baculovirus expressed DUG N protein by Western blotting. When used in an enzyme linked immunoassay (ELISA), the DUG N protein reacted with polyclonal mouse immune ascitic fluids raised against either CCHF or Hazara viruses (both members of the CCHF serogroup of nairoviruses). Cross-reactions between DUG virus (Nairobi sheep disease serogroup) and members of other nairovirus serogroups were not detected.

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