Difference between herpes 1 and 2 simplex virus

For the gold nanoparticles the model of the core—shell spherical nanoparticle was used. The core is gold, the material of nanoparticles. The shell is the stabilizer, which may be described as a thin shell around the gold core. In the calculations we assumed that the shell was homogeneous. It should be noted that all interactions were considered in the presence of visible light, so the values were used for the visible light range.

The nanoparticle shell was variable as it was formed by the stabilizer molecules; its thickness depends much on the nanoparticle size, stabilizer concentration, and material. For the trisodium citrate the shell thickness was around 0. The virus was described as a spherical structure with a nonhomogeneous shell; the surface had some cylindric spikes mainly glycoproteins. The radius of the inner part of the virion in the calculations was equal to 60 nm, and the whole shell thickness was taken as 20 nm: 10 nm of the homogeneous layer and 10 nm the height of the cylinders [ 45 ].

As the dielectric properties were not known exactly for the viruses, we chose the ones for DNA [ 46 ], which was the inner part, and viral proteins and glycoproteins [ 47 ], which corresponded to the shells.

The results of calculations showed the energy of the interaction between the nanoparticle and the virus surface depending on the distance between them. The minimum of the potential indicated the physical adsorption of the nanoparticle on the virus surface, whereas the depth of the minimum indicated the energy of adsorption.

The case with the deepest energy minimum was the most energetically favorable state. Consequently, comparing the potentials for the different relative locations of the virus center and the spike edge, it was seen that the deepest energy minimum and the closest position of the equilibrium system state were for case 1. Similar results were observed for all the nanoparticle sizes considered. However, for the 20 nm nanoparticle these changes were not so obvious.

Comparing the potentials for different nanoparticle sizes it could be seen that the deepest minimum was for the smallest nanoparticles. Hence, it may be supposed that the antiviral effect was higher for the smaller nanoparticles, which was indeed observed in our work. From the results of calculations Figure 4 of the adsorption potential of the systems with different nanoparticle locations, it can be also stated that the nanoparticle adsorption to the virus spike was the most energy-efficient state.

This means that the nanoparticle did not penetrate between the spikes and did not get closer to the virus envelope. Hence, based on the calculation results, it can be hypothesized that the nanoparticles were adsorbed on the virus surface uniformly according to their spikes. This may disturb the viral attachment to the cellular receptors and prevent entry to the cell or fusion with its membrane.

It was seen that nanoparticles likely adsorbed to the virus spikes, as was described previously, which indicated that this process was possibly caused by a dispersion interaction between the nanoparticle and the virus. However, an experimental confirmation on the molecular level that nanoparticle adsorption to the virus spike is the most energy-efficient state was a challenge that was not addressed in this preliminary communication.

Interaction potential between the nanoparticle and the virus depending on the nanoparticle location near the virus spike curve 1 corresponds to site 1 in Figure 3 ; curve 2 corresponds to site 2 in Figure 3 ; curve 3 corresponds to site 3 in Figure 3. Different methods were used to treat the cell monolayers to assess the effect of AuNPs on the inhibition of HSV-1infection: 1 pretreatment assay in which the different AuNPs and HSV-1 were added to the confluent monolayer of Vero cells during or after viral adsorption, and 2 post-treatment assay in which Vero cell monolayers were first infected with HSV-1, and AuNPs were then added to the inoculum at different times.

HSV-1 suspension was incubated with AuNPs for 0 min, 15 min, 1 h, and 4 h, and then added to the Vero cell monolayers. The dose-dependent efficiency of nanoparticles on viral titers released into cell-free culture supernatants was observed.

As shown in Table 1 , incubation of virions with AuNPs I reduced the virus replication in a dose-dependent manner. A higher level of inhibition was observed with nanoparticles of 5. Four-hour pretreatment of the smaller-sized nanoparticles with the virus achieved up to a fold decrease of the HSV-1 load, while bigger-size nanoparticles reduced the viral load twofold, at best, compared to infection control. Pretreatment assay. Vero monolayers were treated AuNPs infected with HSV-1 at different times, and supernatants were titrated on virus replication.

Samples from the supernatant medium were collected at 24 h p. The viral loads in supernatants collected after 48 h p. AuNPs I caused up to a fold inhibition of exogenous virus loads. Because inhibition of viral infectivity could be a consequence of the action of AuNPs inside the cell at a post-entry event, we performed a post-treatment test by adding the nanoparticles at two concentrations 0—24 h after viral infection.

Post-treatment did not have any measurable effect at the concentrations used, so the nanoparticles were not able to reduce the HSV-1 loads data not shown. Depending on the cell type there are two main pathways—non-endocytic and endocytic—of HSV entry into host cells and viruses use a similar set of viral surface glycoproteins to enter host cells.

HSV attaches through the envelope glycoproteins to receptors on the surface of the host cell. This interaction allows for tight anchoring of the virion particle to the plasma membrane of the host cell and eventually leads to membrane fusion and virus penetration into the host cell. Gold nanoparticles probably block the interaction of the virus with the cell, which might be dependent on the nanoparticle size.

The size of the AuNPs may determine the host—pathogen interaction, and smaller nanoparticles may cause higher binding efficiency. It was found that smaller-sized silver nanoparticles AgNPs attach to HSV-1, inhibiting the virus from attaching to host cells and ultimately resulting in attenuation of viral replication [ 48 , 49 ]. Halder et al. It is also possible that gold nanoparticles undergo a size-dependent interaction with HSV These results revealed that AuNPs were capable of controlling viral infectivity, most likely by blocking the interaction of the virus with the cell, which might depend upon the size of the AgNP.

Our results revealed that smaller gold nanoparticles with a size of 10 nm had better antiviral activity, although they showed increased toxicity. NP toxicity strongly depends on their physical and chemical properties, including size and shape.

It was observed that different human cell types were more sensitive to small gold particles 1. It is possible that smaller-sized AuNPs attach more easily to the viral envelope, resulting in the reduction of HSV-1 replication. Smaller-sized nanoparticles were able to inhibit the HSV-1 replication in a pretreatment assay.

It may be hypothesized that AuNP adsorption on the virion may disturb the virus attachment to the cellular receptors and prevent entry to the cell or fusion with its membrane. AuNP adsorption to the virion spikes can be explained by their Van der Waals interaction. Gold nanoparticles with an average size of 10 nm demonstrated inhibitory activities against HSV-1 in a dose- and time-dependent manner at non-cytotoxic concentrations.

Conceptualization, E. All authors have read and agreed to the published version of the manuscript. National Center for Biotechnology Information , U. Journal List Molecules v. Published online Oct 1. Find articles by Edyta Paradowska. Find articles by Iuliia Mukha. Find articles by Nadiia Vitiuk. Zbigniew J. Find articles by Zbigniew J. Brycki, Academic Editor. Author information Article notes Copyright and License information Disclaimer.

Received Aug 26; Accepted Sep This article has been cited by other articles in PMC. Abstract The antiviral activity of nonfunctionalized gold nanoparticles AuNPs against herpes simplex virus type-1 HSV-1 in vitro was revealed in this study. Keywords: antivirals, nanoparticles, HSV-1, near-field mechanism.

Introduction The strong ability of microorganisms and viruses to develop drug resistance is a continuous problem in chemotherapy. Materials and Methods 2. Au Nanoparticles 2. Virus Titration Titration of the viral loads in supernatants was performed by the method of Reed—Muench, and the titer was expressed per mL [ 32 ].

Statistical Analysis Statistics including the mean and standard deviation SD were analyzed with the GraphPad Prism software using a non-parametric unpaired t -test. Results and Discussion 3. Open in a separate window. Figure 1. Nanoparticle Cytotoxicity To rule out the possibility that the reduction of infectivity was caused by the cellular toxicity of AuNPs, monolayers of Vero cells were incubated with different concentrations 0. Figure 2.

Nanoparticle Adsorption on the Virus The first stage of interaction between the virus and the nanoparticles is their physical interaction via dispersion forces.

Figure 3. Figure 4. Figure 5. Antiviral Effect of Nanoparticles Different methods were used to treat the cell monolayers to assess the effect of AuNPs on the inhibition of HSV-1infection: 1 pretreatment assay in which the different AuNPs and HSV-1 were added to the confluent monolayer of Vero cells during or after viral adsorption, and 2 post-treatment assay in which Vero cell monolayers were first infected with HSV-1, and AuNPs were then added to the inoculum at different times.

Table 1 Pretreatment assay. Conclusions 1. Outlook Gold nanoparticles with an average size of 10 nm demonstrated inhibitory activities against HSV-1 in a dose- and time-dependent manner at non-cytotoxic concentrations. Author Contributions Conceptualization, E. Institutional Review Board Statement Not applicable. Informed Consent Statement Not applicable. Data Availability Statement Not applicable. Conflicts of Interest The authors declare no conflict of interest.

References 1. Lauring A. The role of mutational robustness in RNA virus evolution. Piret J. Antiviral drug resistance in herpesviruses other than cytomegalovirus. Irwin K. Antiviral drug resistance as an adaptive process. Virus Evol. Other than stigma and discomfort if you have symptoms, infection with either HSV-1 or HSV-2 brings few long-term health problems for the average healthy adult thankfully.

However, one major exception is HIV transmission. Herpes sores not only provide a way for HIV to enter the body, but even when there are no active lesions, herpes multiplies the types of cells that HIV usually targets, increasing the risk of transmission. To get our top stories delivered to your inbox, sign up for the Healthy Living newsletter. Herpes Simplex 2—and Why the Difference Matters. Herpes Simplex 1 vs. For starters, one is much more likely to be spread through sexual contact.

By Amanda Gardner Updated December 10, Pin FB More. All rights reserved. You can get herpes if you have contact with:.

You also can get genital herpes from a sex partner who does not have a visible sore or is unaware of their infection. It is also possible to get genital herpes if you receive oral sex from a partner with oral herpes. You will not get herpes from toilet seats, bedding, or swimming pools. You also will not get it from touching objects, such as silverware, soap, or towels. If you have more questions about herpes, consider discussing your concerns with a healthcare provider.

Most people with genital herpes have no symptoms or have very mild symptoms. Mild symptoms may go unnoticed or be mistaken for other skin conditions like a pimple or ingrown hair. Because of this, most people do not know they have a herpes infection. Herpes sores usually appear as one or more blisters on or around the genitals, rectum or mouth. The blisters break and leave painful sores that may take a week or more to heal.

Flu-like symptoms e. People who experience an initial outbreak of herpes can have repeated outbreaks, especially if they have HSV However, repeat outbreaks are usually shorter and less severe than the first outbreak. Although genital herpes is a lifelong infection, the number of outbreaks may decrease over time.

STD symptoms can include an unusual sore, a smelly genital discharge, burning when peeing, or bleeding between periods if you have a menstrual cycle. Your healthcare provider may diagnose genital herpes by simply looking at any sores that are present. Providers can also take a sample from the sore s and test it. If sores are not present, a blood test may be used to look for HSV antibodies. Please note: A herpes blood test can help determine if you have herpes infection.

It cannot tell you who gave you the infection or when you got the infection. If you are sexually active, you can do the following things to lower your chances of getting genital herpes:. Be aware that not all herpes sores occur in areas that a condom can cover. Also, the skin can release the virus shed from areas that do not have a visible herpes sore.

For these reasons, condoms may not fully protect you from getting herpes. There is no cure for genital herpes. However, there are medicines that can prevent or shorten outbreaks. A daily anti-herpes medicine can make it less likely to pass the infection on to your sex partner s. Genital herpes can cause painful genital sores and can be severe in people with suppressed immune systems.

If you touch your sores or fluids from the sores, you may transfer herpes to another body part like your eyes. Do not touch the sores or fluids to avoid spreading herpes to another part of your body.

If you do touch the sores or fluids, quickly wash your hands thoroughly to help avoid spreading the infection. If you are pregnant, there can be problems for you and your unborn fetus, or newborn baby.