GANCICLOVIR

Andi Cahyadi

Ganciclovir is a guanosine nucleoside analogue, homologue Acyclovir and the first antiviral drug effective in treating cytomegalovirus in humans. Ganciclovir inhibits not only herpes virus but also the transformation of lymphocytes by the Ebstein Barr Virus. (Crumpacker, 1996; Marshall and Koch, 2009)

Mechanisms and How to Work Ganciclovir

Ganciclovir in vivo transformed into Ganciclovir triphosphate which inhibits viral DNA polymerase, including Herpes Simplex Virus and CMV, by way of competitive inhibitors on deoksiguanosine triphosphate formation in viral DNA elongation. (Marshall and Koch, 2009) After removing pyrophosphate, Ganciclovir monophosphate binds to the end of the formation thereby inhibiting replication of DNA chains. (Crumpacker, 1996) Unlike acyclovir, Ganciclovir is not an absolute chain terminator so that the sub-genomic fragment of CMV remains synthesized in short segment. All antiviral drugs work because of its ability to inhibit CMV DNA synthesis and inhibits elongation in DNA replication. In the cells infected with herpes simplex virus, thymidine kinase phosphorylate the virus into a form Ganciclovir monophosphate and cellular enzymes further modify Ganciclovir Ganciclovir monophosphate to triphosphate which can inhibit viral DNA synthesis. (Crumpacker, 1996)

CMV does not have the enzyme thymidine kinase homologous and as an alternative is to phosphorylate UL97 gene product Ganciclovir. CMV UL97 kinase gene insertion into the vaccinia virus Ganciclovir incentives make recombinan virus susceptible to Ganciclovir. (Crumpacker, 1996)

Left half Ganciclovir triphosphate in CMV-infected cells was 16.5 hours compared to acyclovir triphosphate which is only 2.5 hours. In the circumstances molar base, Ganciclovir not as effective as acyclovir triphosphate as a DNA polymerase inhibitor, but the concentration of CMV in CMV-infected cells ten times greater than with acyclovir. Ganciclovir triposfat high levels and a long intracellular half-life makes Ganciclovir is considered to be superior compared with acyclovir in inhibiting replication of CMV. (Crumpacker, 1996; Marshall and Koch, 2009)

 Pharmacokinetic and Toxicity of Ganciclovir

Giving intravenous Ganciclovir 5 mg/kg in one hour produces the peak concentration in serum 8.3 g/ml at the end of infusion. Ganciclovir in the plasma half-life was 2.9 hours and the average clearance of 3.9 ml per kilogram per minute. Twelve hours after the infusion, serum concentrations of less than 0.5 ug/ml. Regimen from 7.5 to 10.0 mg Ganciclovir per kilogram of body weight divided in 2 doses per day will produce peak serum concentrations from 4.5 to 10 ug/ml. Ganciclovir had the blood brain barrier penetration to produce a concentration in cerebrospinal fluid 0.7 ug/ml when measured simultaneously in plasma levels of 2.2 ug/ml within 3.5 hours after administration of intravenous 2.5 mg/kg. After treatment with Ganciclovir 1000 mg orally 3 times per day, maximum and minimum concentration in plasma was 1.2 and 0.2 ug/ml. Ganciclovir oral bioavailability is between 6-9%. Serum concentration has been entered in the ED50 in most isolates of CMV (0.2 to 1.6 g/ml). (Crumpacker, 1996)

Ganciclovir causes granulositopenia, thrombocytopenia, azoospermia and increased serum creatinine. Patients with CMV retinitis treated with intravenous Ganciclovir 3 months, 40% will have granulositopenia (neutrophil count <1000 per cm3) and 15% had thrombocytopenia <50,000 cm3. Granulositopenia and thrombocytopenia did not look after Ganciclovir was stopped except for one patient who suffered irreversible neutropenia and Pseudomonas sepsis. Anemia may also appear on the long-term treatment. The incidence of thrombocytopenia and granulositopenia on oral administration is rare than intravenously. Granulositopenia can be prevented by giving recombinant granulocyte colony stimulating factor or granulocyte macrophage colony stimulating factor. Patients will have a lower granulositopenia episode. (Crumpacker, 1996)

Twenty percent of the 20 people who received bone marrow transplant will experience an increase in serum creatinine over 2.5 mg/dl (221 μmol per liter) after 120 days of intravenous Ganciclovir. Serum creatinine returned to normal after Ganciclovir was stopped. Ganciclovir is more dangerous when used in conjunction with a toxic drug in the bone marrow such as zidovudine. Eighty percent of the 40 people require a dose reduction because of hematological toxicity of Ganciclovir and zidovudine. (Crumpacker, 1996) azoospermia associated with the provision of Ganciclovir on animal studies due to a direct effect on sperm production constraints. Testicular endocrine function is not affected but the data on experimental animals showed suppression of fertility may occur. (Crumpacker, 1996)

Clinical Use Ganciclovir

Ganciclovir inhibits the growth of CMV from laboratory isolates and clinical isolates with plasma concentrations of 0.1 to 1.6 ug / ml. (Crumpacker, 1996) Ganciclovir is more active than acyclovir in inhibiting replication of CMV. In tissue culture, Ganciclovir has antiviral activity against viruses amazing Herpes Simplex type 1 and 2, Varicela Zoster virus, Ebstein-Barr Virus and Human Herpes Virus 6. (Crumpacker, 1996) Ganciclovir is less effective against human adeno virus, human papilloma virus, Influenza virus and other RNA viruses. (Crumpacker, 1996; Marshall and Koch, 2009)

Ganciclovir is a synthetic nucleotide analog guanosine acyclik, phosphorylated to triphosphate in the cell and acts as an inhibitor of viral DNA synthesis. In preliminary data, it is effective for treating symptomatic CMV. (Whitley et al, 1997) Phase II study, Ganciclovir showed improvement or stabilization of hearing 4 of 30 infants with congenital CMV infection are symptomatic after 6 months or more. (Whitley et al, 1997) During the treatment period, expenditure decreased quantitatively virus in urine, but after treatment, again as in earlier viremia before treatment. (Leung et al, 2003) phase III randomized study, Ganciclovir beneficial in children with severe congenital CMV infection. (Pass, 2002) central nervous system damage that has occurred can not be repaired but the damage can be prevented before they happen. Ganciclovir for the treatment of lost hearing in children with CMV asipmtomatik is rare. (Leung et al, 2003) Ganciclovir Side effects include bone marrow suppression and toxic to the gonads should be a lot of rethinking. (Numazaki and Chiba, 1997), but not enough data to decide termination of the use of Ganciclovir in the treatment of neonatal CMV hepatitis

 

REFERENCES

 Whitley R, Cloud G, Gruber W, Storch GA, Demmler GJ, Jacobs RF, et al. Ganciclovir treatment of symptomatic congenital cytomegalovirus infection: Results of a phase II study. J Infect Dis. 1997; 175: 1080-1086.

Marshall BC, Koch WC. Antivirals for cytomegalovirus infection in neonates and infants: focus on pharmacokinetics, formulations, dosing, and adverse events. Paediatr Drugs. 2009;11(5):309-21.

Crumpacker, CS. Ganciclovir. New Engl J Med 1996;335:721–729.

Numazaki K, Chiba S. Current aspects of diagnosis and treatment of cytomegalovirus infection in infants. Clin Diagn Virol. 1997; 8: 169-181.

Leung AKC, Sauve RS, Davies D. Congenital Cytomegalus Infection. J Natl MedAssoc. 2003;95:213-218.)

Pass RF. Cytomegalovirus infection. Pediatr Rev 2002; 23:163-169.

GB Virus C (GBV-C) - Hepatitis G Virus

Andi Cahyadi

History

            In 1967, from a surgeon with the initials GB who suffered from acute hepatitis, GB virus can be isolated and the experiments successfully transmitted to the tamarin monkey (Masuko et al., 1996). Then two new virus can be isolated which is a positive strand RNA viruses including Flaviviridae family, namely GB virus type A (GBV-A) and GB virus type B (GBV-B) (Simons et al., 19 951). It turned out that GBV-A and GBV-B is only found in the tamarin monkey (Alter et al, 1996).

            Leary et al. in 1996 found another virus that GBV-C in patients with acute hepatitis, chronic and healthy people who live in the United States, Canada and Africa. GBV-C is found in people with risk of exposure to viral hepatitis, including exposure to non-AE viral hepatitis (Alter et al, 1996). In the same year successfully isolated a new virus called hepatitis G virus (VHG) from patients with chronic hepatitis in the United States (Linnen et al., 19 961). GB virus C (GBV-C) and Hepatitis G Virus (HGV) is a fairly new virus in humans, which was found by two different research groups. Both the virus was identified from patients with hepatitis caused by viruses. As well as the Hepatitis C virus (HCV), VHG and GBV-C has the same amino acids and nucleotides more than 95% and 85%, so the second concluded the virus originated from the same virus species with different isolates (Retno et al., 2000 .) For further discussion both virus called GBV-C.

The structure of GBV-C

GBV-C including the family Flaviviridae, which consists of single stranded RNA molecules and has approximately 9500 nucleotides (Sherlock, 1999). Twenty-five percent of GBV-C has the same amino acid with HCV, and the nature kronisitasnya quite prominent in human infection. Genome as a whole pattern similar to VHC and other Flavivirus (In Bisceglie, 1996). This virus is unique among Flafiviridae because it does not encode a protein that resembles the core (core like protein) which is a protein that is located near the amino end of poliprotein virus.

Complete genome sequence of the isolated HGV and GBV-C has now been determined. Both are positive strand RNA virus which in fact has almost the same nucleotide sequence. HGV amino acids and GBV-C has a 29% homology with HCV, which indicates that the virus is different and not the serotypes of HCV. HGV and GBV-C has the amino acid homology of 48% with GBV-A and 28% with GBV-B. In the conversations that HGV and GBV-C will be referred to as GBV-C. GBV-C has two kinds of protein that is 2 structural proteins (E1 and E2 proteins) and 5 non-structural proteins (proteins NS2, NS3, NS4, NS5A and NS5B) (Tillmann et al., 2001) (Figure 1). E2 protein is a key protein that can stimulate the formation of antigen in the body.

GBV-C can be bred (inoculated) into the body of primates such as chimpanzees, and macaques tamarin. Also, studies Tan et al. (2002) showed that this virus can be duplicated in vitro by inoculation into the PBMCs (Peripheral Blood mononuclear cell). This is a good omen that in the future pengembangbiakkkan GBV-C is feasible.

  
Prevalence and GBV-C Transmission Line

GBV-C can be transmitted through blood and blood products, sexual contact, and vertically from mother to fetus. GBV-C also can be transmitted through infected serum in animal primates, including the tamarin, chimpanzee and macaque monkeys. GBV-C was detected in many drug users of intravenous drugs. The prevalence of GBV-C differ in various populations. Centers for Disease Control and Prevention has found among patients in the United States are diagnosed with hepatitis non-A, non-B of approximately 18% are positive GBV-C RNA in which the majority of patients (80%) were also infected with HCV (DiBisceglie, 1996; CDCP, 1996),

GBV-C infection can occur in healthy blood donors (Linnen et al., 19 962). The prevalence of GBV-C infection in blood donors in Surabaya, Indonesia at 2.7%. While the prevalence of GBV-C infection and coinfection with HCV that occurs in patients with chronic liver disease in Surabaya by 8.4% (Retno et al., 2000).

GBV-C infection is found widely in the world and easily transmitted by transfusion or other parenteral route. Because GBV-C infection is mainly through the parenteral route, then the patients who are undergoing hemodialysis have a high risk to be infected with GBV-C (Linnen et al., 19 961). About 3% of kidney dialysis patients have GBV-C RNA in their blood (Masuko et al., 1996) but other researchers found a higher prevalence (Tanaka et al., 1996).

High risk groups in the transmission of GBV-C is the commercial sex workers and homosexual men. In Taipei, Taiwan, 21% female commercial sex workers without a history of intravenous drug use found GBV-C RNA positive. Seroprevalence of GBV-C RNA in a positive homosexual men infected with HIV in Frankfurt, Germany, was 8.5%. The same researchers analyzed the antibodies against the envelope glycoprotein E2 (E2Ab) of GBV-C and found the prevalence overall of 31.9%. In Spain, the prevalence of GBV-C RNA has been reported by 13.4% and 19%. 51% of HIV-infected homosexual men in Scotland showed GBV-C RNA positive and 4 of the 17 negative samples, the PCR became positive. Transmission through sexual contact plays an important role in the development of a relatively new biological viruses found this. History of sexually transmitted diseases was significantly associated with GBV-C infection before (Wacthler et al., 2000).

Diagnosis of GBV-C

Specific diagnosis according to type of virus that causes can only be determined through laboratory examination (Hardie, 2005). Diagnosis of infection with GBV-C is done by examination of Polymerase Chain Reaction (PCR) is to detect viral RNA in serum, tissue or other infected fluid. PCR is still the superior method available today for diagnosis of infection with GBV-C. Possible mismatch PCR test results with the prevalence of GBV-C infection can occur in people who have recovered from infection or at the time did not contain GBV-C again (In Bisceglie, 1996).

Clinical Aspects of Infection with GBV-C On The Body

Unresolved issue is whether GBV-C cause hepatitis or other diseases. Because infection with GBV-C and HCV is associated then it becomes difficult to analyze the effect of GBV-C itself. Among patients with GBV-C infection that developed into hepatitis, liver damage is not severe and often appear lighter than HCV infection alone (Tanaka et al., 1996).

Tanaka (1996) examined 189 patients who had symptoms such as chronic hepatitis C and found 21 people (11%) carrying GBV-C RNA in serum. However, less than 20% of patients with cirrhosis cryptogenik or other forms of chronic hepatitis of unknown cause was also infected with GBV-C. Determination of GBV-C is still difficult because of the chronic course of illness largely GBV-C along with another hepatitis virus infection. Thomas et al. (1997) showed that GBV-C only as an innocent bystander virus (the virus that are not influential broadcaster.) This can be proved through the examination of histology and biochemistry of people with GBV-C positive and GBV-C negative. In both groups found no significant difference in liver histology and serum transaminase enzyme elevations. It also found significant differences in GBV-C infection of immunocompetent people and imunokompromise (Pessoa et al., 1998).

Since wearing serologic HBsAg and anti-HCV as a filter for blood donors, the incidence of post-transfusion hepatitis declined rapidly. But examination screened for HBsAg and anti-HCV does not reduce the risk of infection with GBV-C, although it showed some blood recipients had been infected with HCV and GBV-C before transfusion done, so need to test strain of GBV-C alone (Tillman et al., 2001) .

There are unique clinical course of GBV-C infection. With a mechanism that remains unknown, GBV-C could be free of the immune response in the human body. There is evidence to support this statement: First, GBV-C could survive long in the human body to more than 10 years. Second, during GBV-C RNA positive, in human blood can not find the presence of antibodies against GBV-C E2 protein. Vice versa when a person recovers from infection with GBV-C (not found GBV-C RNA in the blood) appear before antibodies to the E2 protein. Third, GBV-C merupkan low density particle that has a low immunogenic power.

Management of acute GBV-C together with other acute viral hepatitis, ie a total break with a diet low in fat and high in protein and enough calories. Provision of interferon (IFN) of 5 million units every day or 10 million units 3 times a week for at least 6 months to suppress replication of GBV-C, but almost all cases of relapse after IFN α discontinued (Karayiannis et al., 1997). Given that little research is currently ongoing and still being a few studies on GBV-C, then a rational pharmacotherapy recommendations for GBV-C has not been issued. (Nurjanah, 2001). Hepatoprotector preparations (such as schizadrine, curcuma, Fructus, ginseng) can be used on GBV-C infection because it has a working cell and protection against liver function

REFERENCES

Alter HJ. 1996. The cloning and clinical implications of GBV-C and HGBV-C [Editorial]. N Engl J Med.;334:1536-7.

CDCP. 1996. Hepatitis Surveillance, CDC Report Number 56. Centers for Disease Control and Prevention, Atlanta, GA

DiBisceglie A. 1996. Hepatitis G Virus Infection: A Work in Progress Annals of Internal Medicine, 1 November. 125:772-773.

Hardie D. 2005. Notes which were prepared by Diana Hardie for Virology Lectures to 3rd Year Medical Students in the Department of Medical Microbiology, University of Cape Town. http://www.uct.ac.za/depts/mmi/jmoodie/dihep.html. Akses tanggal 4 Maret 2005 jam 15.00

Karayiannis, S.J. Hadziyannis, J. Kim, J.M., et al, 1997. "Hepatitis G Virus Infection: Clinical Characteristics and Response to Interferon". Journal of Viral Hepatitis, Volume 4, No. 1, 37-44.

Linnen J, Wages J Jr, Zhang-Keck ZY, et al¹. 1996. Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent. Science.;271:505-9.

Linnen J, Wages J Jr, Zhang-Keck Z-Y, et al². 1996. Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent. Science;271:505-508.

Masuko K, Mitsui T, Iwano K, et al. 1996. Infection with hepatitis GB virus C in patients on maintenance hemodialysis. N Engl J Med.;334:1485-90.

Nurjanah. 2001. Therapy for Chronic Viral Hepatitis. J Gastroenterol Hepatol, 2:28-35

Pessoa MG, Terrault NA, Detmer J, et al. 1998. Quantitation of hepatitis G and C viruses in the liver: evidence that hepatitis G virus is not hepatotropic. Hepatology;27:877-880.

Retno H et al. 2000. Epidemiologi dan Distribusi Genotipe Virus Hepatitis G. Kumpulan Seminar Ilmu-ilmu Biomedis Mutakhir : Yogyakarta.

Retno H. 1999. Prevalence of GB Virus C/Hepatitis G Virus Infection Among Various Population in Surabaya, Indonesia and Identification of Novel Groups of Sequence Variants. Journal of Clinical Microbiology; 38, 2:662-668

Sherlock S. 1999. The hepatic flaviviridae: summary. J Viral Hepat;6:Suppl 1:1-5.

Simons JN, Leary TP, Dawson GJ, et al¹. 1995. Isolation of novel virus-like sequences associated with human hepatitis. Nat Med;1:564-569.

Tan D et al. 2002. In Vitro Infection of Human Peripheral Blood Mononuclear Cells by GB Virus C/Hepatitis G Virus. The New England Journal of Medicine 2004. Volume 345:715-724

Tanaka E, Alter HJ, Nakatsuji Y, et al. 1996. Effect of hepatitis G virus infection on chronic hepatitis C. Ann Intern Med.;125:740-3.

Thomas DL, Vlahov D, Alter HJ, et al. 1998. Association of antibody to GB virus C (hepatitis G virus) with viral clearance and protection from reinfection. J Infect Dis;177:539-542.

Tillman et al. 2001. Infection with GB virus C and reduced mortality among HIV Infected Patients. N Engl J Med, 345:715-21

Wächtler M, Hofmann A, Müller G, et al. 2000. Prevalence of GB virus C/hepatitis G virus RNA and anti-E2 glycoprotein antibodies in homosexual men with HIV coinfection. Infection;28:297-300.

PAPUA NEW GUINEA

Bagian Pertama
PERJALANAN MENUJU JAYAPURA
Andi Cahyadi

Papua Nugini atau Papua New Guinea atau PNG, negara di sebelah timur Pulau Papua yang dahulu dikenal dengan Irian Jaya. Negara PNG masuk dalam wilayah Benua Australia meskipun secara geografis terpisah. 

Bagian sisi timur dan utara PNG berbatasan dengan laut dan negara Oseania. Ibu kota Negara berada di Port Moresby. Masyarakat dan budaya di sana sangatlah mirip dengan saudara kita di Papua, mulai dari warna kulit dan kebiasaan.

 (http://www.operationworld.org/papu)

Inilah pertama kali saya ke luar negeri meskipun hanya ke Papua Nugini

 Papua Nugini memiliki lebih dari 800 bahasa daearah lokal dengan populasi yang hanya sekitar 6 juta jiwa. Bandingkan dengan Indonesia yang bependuduk lebih dari 200 juta jiwa. Penyebaran penduduk di PNG terpusat pada sebagian kecil wilayah dan tersebar di perkampungan perkampunga yang mana 18-20% nya saja di perkotaan. Penduduk di Indonesia terpusat di perkotaan dan terpusat sebagian besar di Pulau Jawa. Anak-anak di sana juga ceria seperti anak-anak di Indonesia terutama saat ada festival budaya dimana mereka bisa berdandan dengan bunga bunga.

 (http://www.papuanewguinea.travel)

Tetapi jangan salah, foto di bawah ini bukanlah orang PNG tetapi teman-teman saya dari Papua juga (dari Jayapura). Sekilah mereka sangat mirip dengan warga PNG karena mereka memiliki nenek moyang yang sama. Yang kecil keriwul di depan itu namanya Echi, tinggalnya di Kabupaten Teluk Bintuni di Papua Barat bersama mamaknya yang berkaos putih, namanya Suster Natalia. Yang lain adalah sepupu dan keponakannya. Senang sekali rasanya bisa berkenalan dan bercanda bersama mereka.

PERJALANAN AWAL PAPUA NUGINI

Sebagai negara yang berbatasan darat dengan Indonesia, sudah selayaknya kita perlu mengenal lebih dekat PNG. Perjalanan ke PNG dimulai dengan perjalanan ke Jayapura, ibukota Provinsi paling timur Indonesia yaitu Provinsi Papua. Dahulu hanya ada provinsi Irian Jaya tetapi sekarang dipecah menjadi dua yaitu Provinsi Papua beribukota di Jayapura dan Provinsi Papua Barat beribukota di Manokwari. Perjalanan ke Jayapura hanya bisa ditempuh lewat laut dan udara saja. Untuk kali ini, saya akan mencoba perjalanan lewat udara. 

Perjalanan ke PNG dimulai dari penerbangan menuju Jayapura melewati Sorong atau Manokwari di Papua Barat. Manokwari adalah ibukota Provinsi Papua Barat. Pesawat juga dapat transit di Biak. Khusus yang ingin bersantai, jangan lupa mencicipi abon gulung khas Sorong dan Manowari. Meskipun harganya sedikit mahal, tetapi rasanya akan bikin ketagihan. Rasa daging sapi atau ayam atau ikannya begitu terasa.

Abon Gulung Hawai khas Manokwari

(http://dherdian.wordpress.com/2012/10/23/abon-gulung-manokwari/)

Sepanjang perjalanan udara dari Manokwari sangatlah indah melewati pesisir utara Pulau Papua. Membentang pantai yang indah dengan hamparan pulau kecil hijau kebiruan. Sangat indah ciptaan sang pencipta. Beberapa kabupaten akan dilewati mulau dari kabupaten Manokwari, Teluk Bintuni, Teluk Wondama, Nabire, lalu memasuki Teluk Cenderawasih dengan Pulau Biaknya. Berikut ini adalah beberapa keindahan laut pantai utara Pulau Papua.

 

 

 

 

Bagi yang transit di Biak, kita bisa menikmati bandara internasional peninggalan jaman perang dahulu. Berikutnya kita akan tiba di Kabupaten Sarni dan memasuki kabupaten Jayapura baru memasuki kota Jayapura. Sebelum turun ke Jayapura, nikmatilah keindahan Danau Sentani yang melegenda, danau terbesar di papua. Pesawat akan menukik mengelilingi indahnya danau dengan bukit bukit kecil yang menawan. Deretan rumah penduduk juga akan berjajar rapi. Ohya sekedar diketahui, deretan rumah yang tertata rapi itu adalah daerah transmigrasi dari Jaa. Jadi kita orang di sana serasa pulang kampung saja.

 

 

 

 

Kita juga bisa menikmati indahnya danau Sentani sebelum pesawat tiba di Bandara Sentani Jayapura. Danau tersebut bertepi nan berkelok-kelok dikelilingi perbukitan rumput yang indah. Suber dari WIKI,

Danau Sentani adalah danau yang terletak di Papua Indonesia. Danau Sentani berada di bawah lereng Pegunungan Cagar Alam Cycloops yang memiliki luas sekitar 245.000 hektare. Danau ini terbentang antara Kota Jayapura dan Kabupaten Jayapura, Papua. Danau Sentani yang memiliki luas sekitar 9.360 hektare dan berada pada ketinggian 75 mdpl. Danau Sentani merupakan danau terbesar di Papua.

Di danau ini juga terdapat 21 buah pulau kecil menghiasi danau yang indah ini. Arti kata Sentani berarti "di sini kami tinggal dengan damai”. Nama Sentani sendiri pertama kali disebut oleh seorang Pendeta Kristen BL Bin ketika melaksanakan misionaris di wilayah danau ini pada tahun 1898.

 

Barulah kita tiba di Bandara Internasional Sentani di Jayapura. Bandara ini termasuk padat tetapi tertata rapi dan bersih. Masyarakatnya juga ramah menyambut kedatangan kita. Jangan khawatir, disini kita akan menemukan seluruh suku di Indonesia, ada masyarakat Jawa, Maluku, Sulawesi dan penduduk lokal yang jumlahnya lebih sedikit. Memang sih tidak semegah dan selengkap Bandara Internasional Juanda di Surabaya tetapi cukup nyaman kok disana. Pegunungan di balik Bandara tersebut adalah Bukit di Pinggir Danau Sentani. Tetapi tidak perlu takut, meskipun dikelilingi bukui, Bandara Sentani Jayapura tidak semenakutkan Bandara Husein Sastranegara di Bandung kok.

 

 

 

 

Kembali ke cerita PNG. Perjalanan dari Bandara Sentani di Jayapura ke PNG tidak terlalu jauh, paling hanya dibutuhkan sekitar 2 jam saja dari Kota Jayapura. Setelah sebelumnya melihat Danau Sentani dari udara, sekarang tiba saatnya melihat keindahan danau dengan menyusuri tepinya. Perjalanan dimulai dari menyusuri Danau Sentani di wilayah Kabupaten Jayapura sampai memasuki Kota Jayapura. Danau Sentani sangatlah indah terutama di siang hari. Jalannya berkelok kelok dengan pemandangan bukit yang indah.

 

 

 

 

 

 

 

 

 

Ohya tambahan informasi saja. Di salah satu sisi Danau Sentani ada perkampungan penduduk yang masing-masing rumah ada namanya. Penghuninya juga cantik-cantik. Setiap hari mereka terlihat senang karena selalu ada berbagai musik di sana terutama musik dangdut dan house musik. Kalau malam tampak terang bernderang dengan lampu yang berwarna warni. Kita bisa berkenalan dengan orang Jawa, Menado, Bugis, Ambon, Makasar, Medan dan seluruh suku di nusantara. Tetapi sayang, tempay itu adalah lokasi seperti yang di Surabaya yang telah ditutup beberapa waktu lalu oleh Ibu Risma, walikota Surabaya.

Ketika tiba di Jayapura, jangan lupa singgah dan menikmati indahnya malam di sana. Jangan khawatir, makanan dan minuman seperti nasi goring dan tempe penyet serta soto melimpah ruah di sana. Jadi anda tidak perlu bersusah payah.

 

Hotel dan penginapan juga banyak ditemui mulai dari kelas melati sampai bintang empat. Tetapi tentu saja dengan harga makanan yang lebih mahal. Setelah beristirahat, esok paginya barulah melanjutkan perjalanan ke PNG. Cerita selanjutnya tentunya perjalanan di Papua Nugini.